What I did before

When I started treating breast cancer, systemic therapy recommendations were usually based only on the menopausal status of the woman and whether there was cancer in the axillary nodes.  Although estrogen status was being measured the importance of this marker was not appreciated.

What changed my practice

In the last decade there has been an explosion of information about the genetics and molecular makeup of breast cancers with a heightened understanding that breast cancer is not one disease. A landmark publication in 2000 described four types of breast cancer. ¹ In a recent as yet unpublished study using newer sequencing technology, researchers at the BC Cancer Agency and collaborators from the UK have suggested 9 distinctive types of the disease. ²  The recognition of these subtypes of breast cancer is changing how we approach and treat the disease.

The risk of recurrence is a major concern when an early breast cancer is diagnosed as even with excellent surgery there is a risk of both local and systemic recurrence.  Architectural factors such as the size of the tumour and nodal involvement have classically been used to determine risk. Biological features such as estrogen receptor status, HER2 expression and grade, often measured by Ki67, are now being included in our risk assessment.

The responsiveness of the tumour has also become an important determinant in how we treat the disease.  Responsiveness describes how the tumour will be affected by specific treatments.   For example, estrogen receptor status determines whether a breast cancer will respond to endocrine therapy; the gene HER2 is associated with response to anti HER2 therapy such as trastuzumab (Herceptin); and high KI67 tumours may be more responsive to chemotherapy than those with a lower grade or KI67.  Thus two similar sized tumours may get different treatment recommendations based on their biology.

What I do now

For patients with low grade estrogen receptor positive tumours I am recommending much less chemotherapy even if there is nodal involvement and/or the woman is premenopausal.  In these tumours, endocrine therapy may be the most effective treatment and chemotherapy may minimally impact survival.  Having said that, some patients still benefit from including chemotherapy in addition to hormone therapy.  For patients with HER2 overexpressing tumours I often recommend chemotherapy and trastuzumab even if the tumour is small with no involved nodes.  Understanding the biology of breast cancers is providing more personalized recommendations and this is translating into better outcomes.

As we further define subtypes, more targeted treatments will be developed but at this time for many cancers we continue to give broad cytotoxic therapy.  As well, new agents are being developed and may be further decrease recurrences. We are also now frequently rebiopsying recurrent cancers to further understand the markers of response and resistance and to tailor treatment. We also need to study the “host” patient, as the pharmacogenomics of the individual may affect how the drug is metabolized and also may contribute to the effectiveness and the toxicity of the therapy.

How does this affect family physicians?  Treatment recommendations may be more complicated so counseling patients prior to their oncological consultation may be more confusing.  It may be more difficult to know whether chemotherapy will be recommended or not especially if we begin to do more complex assessments of tumours in specialized laboratories. Numerous studies are reported in the lay and academic press and are never substantiated.  Understanding what is of relevance to the care and management of our patients and which data is transient is difficult.  We need to ensure that the government prioritizes an upgrade of our electronic BC Cancer Agency website and electronic record to make it accessible to primary health care providers with the appropriate, evidence based results.

Biological information is often available as soon as the core biopsy diagnoses an invasive cancer.  Early referral to centres with multidisciplinary teams may avoid long delays and confusing information for both the patient and the primary care providers.  Electronic integrated systems may also aid the transfer of information. Frequent updates at family practice meetings and in journals can also provide current treatment and care models to a wider audience.  With this knowledge, family practices can provide a broad idea of the concept of adjuvant therapy for the treatment of early breast cancer and introduce the idea of chemotherapy, hormones and radiation without specifying the details.  Family doctors should be aware of the new patient package, including a patient book that is available through the Alliance for Breast Cancer Information at the BC Cancer Agency. ³ Reassuring patients about the improvements in survival as over 90% of early breast cancer cases in BC now live over 5 years will also help provide helpful information to decrease a woman’s anxiety. 4

References (Note: Article requests require a login ID with CPSBC or UBC)

1. Perou CM, Sorlie T, Eisen MB, et al.  Molecular portraits of human breast tumours.  Nature 2000; 406 (6797): 747-52 (View article with CPSBC or UBC)
2. Personal communication with Dr Samuel Aparicio
3. Alliance for Breast Cancer Information BC, 604 707 5818, and Intelligent Patient Guide – Olivotto, Gelmon, McCready, 5^th edition, 2011 (book)
4. Coleman MP, Forman D, Bryant H et all.  Cancer survival in Australia, Canada, Denmark, Norway, Sweden and the UK, 1995-2007 (the international cancer benchmarking partnership): an analysis of population –based cancer registry data.  Lancet 2011; 377(9760): 127-138. (View article with CPSBC or UBC)

Cancer Care Outreach Program on Education (CCOPE)

Over the past 4 months, UBC CPD in partnership with BCCA and FPON has been delivering case-based workshops on breast cancer care to various communities in BC, the last workshop is scheduled for Dawson Creek on March 28^th.  Workshop contents covers screening guidelines, diagnostic procedures, main treatment options and their potential side effects, and follow-up of breast cancer patients.

Read more about the Cancer Care Outreach Program on Education (CCOPE) .

Read more about CCOPE – Breast Cancer Community Workshops.

What I did before

Cerumen build-up is a common problem for patients and doctors alike. According to McCarter et al cerumen impaction is present in approximately 10 percent of children, 5 percent of normal healthy adults and up to 57 percent of older patients in nursing homes (1). If not managed well, this can result in persistent wax build-up (or impaction) for patients and added time to a busy physician’s office – sometimes without effective resolution in the short term. For patients this can sometimes result in sensation of blocked ears, pain and even hearing loss.  I previously spent more time cleaning wax in the office, but less so as time went by. This has been an evolution in my practice for over a decade or more, where previously curetting and vacuuming was a regular occurrence in my clinical office. In the case of Family Physicians, syringing is often utilized, which is time-consuming and cumbersome, and sometimes without the desired response. Counseling patients on preventative measures for wax build-up was something I did not routinely do in the past, spending more time on the management of the problem.

What changed my practice

Wax build-up is a bothersome problem for patients and this is, for the large part, preventable. The more time I spent on explaining to patients how to care for their ears and related wax build-up, the less wax problems I encountered in the office. I also took for granted that patients knew that cotton buds are not for use in the external canals – a major factor contributing to wax impactions as well as potentially having more serious morbidity. I, not infrequently, saw patients in the office with a piece of cotton bud broken off in the ear, and occasionally a perforation that resulted from cotton bud trauma. The more I regularly spoke with patients about this basic subject, I more I realized that many patients did not appreciate the improper use of cotton buds. I also began to understand the misperception that water is not good to get in the ears (it is only contraindicated in a small population of people for specific reasons).

What I do now

The literature is not clear as to whether using cerumenolytic drops are beneficial to water alone (2,3) . For all patients presenting with wax related problems, I take the time to talk about aural hygiene. Providing there are no contraindications (eg. perforation or infection), I talk about the value of self-irrigation of the external ear canals with water and to refrain from using cotton buds. I show them how to aim their ear up towards the shower head to let water in the ear, and then tilt the head down to enable water run out. This can be followed by gentle use of facial tissue externally in the ear. For those individuals that bath instead, particularly in the case of children, I explain how to flush the ears with the help of a small cup or bulb syringe. Rinsing the ears, as mentioned above, can be performed with each shower/bath, or as frequently as patients desire. I usually recommend self-rinsing two to three times per week – keep in mind that this is not an exact science so these are my personal suggestions. For those patients who present in my office with unrelated ENT problems and I see that wax build up is, or can be, an issue, I always try to remember or make the time to provide them with this basic information on aural hygiene. I also, at whatever opportunity I can, speak with learners and practitioners about this common clinical scenario.

References (Note: Article requests require a login ID with CPSBC or UBC)

1. McCarter DF, Courtney AU, and SUSAN M. Pollart SM, Am Fam Physician. 2007 May 15;75(10):1523-1528. http://www.aafp.org/afp/2007/0515/p1523.pdf
2. Burton MJ, Doree C. Ear drops for the removal of ear wax. Cochrane Database Syst Rev. Jan 21 2009;CD004326. (View article with CPSBC or UBC)
3. Cerumen Impaction Removal: http://emedicine.medscape.com/article/1413546-overview

What I did before

Until recently, the standard approach to managing type 2 diabetes consisted of “lifestyle” (diet and exercise) therapy, along with metformin, followed by either sulfonylurea (glyburide or gliclazide), or TZD (rosiglitazone or pioglitazone), and eventually insulin, depending on the circumstance (1). In the last few years, the use of TZDs has declined; mostly reflecting the recognition of potential side effects, such as weight gain, edema, and possible cardiovascular effects of rosiglitazone (2). At the same time, a new class of agents, incretins, has emerged, with both real and potential advantages over previous agents (3). However, as with any new class of agents, long term follow-up will be required before we can fully understand the role (including risks and benefits) of these new agents.

What changed my practice

Incretins utilize the physiologic effects of a gut hormone, Glucagon-like peptide-1 (GLP-1), to augment pancreatic insulin secretion, thereby lowering blood glucose. One group of agents [DPP-4 inhibitors: sitagliptin (Januvia®), saxagliptin (Onglyza®), linagliptin (Trajenta®)], blocks the rapid breakdown of natural GLP-1, by inhibiting the enzyme DPP-4. These oral agents, administered once daily, augment endogenous GLP-1, resulting in an A1C reduction of 0.5 – 0.9%. Since GLP-1 does not directly stimulate insulin, they have the advantage of not promoting hypoglycemia or weight gain. Another approach uses peptides with similar effects as GLP-1, but which are not degraded as quickly. These so called “incretin mimetics” include liraglutide (Victoza®) and exenatide (Byetta®) and are administered by subcutaneous injection, once or twice daily, respectively. In addition to augmenting insulin secretion, the incretin mimetics can slow gastric emptying, reduce appetite and promote weight loss, which can further improve metabolic control (approximate A1C reduction: 1 – 1.5%). For individuals in whom weight gain is a particular concern, these added benefits can outweigh the disadvantages of injection therapy. There may be additional effects, including improving surrogate markers of CV risk such as blood pressure, and lipids, but it is not clear whether these effects are clinically significant. The primary dose-limiting side effect of the incretin mimetics is nausea, which often improves with time. Other possible (though rare and not proven) side effects include risks of pancreatitis and thyroid c-cell hyperplasia observed in rodents, but is not clear whether these occur more frequently in humans (4).

What I do now

Since the advent of incretin therapy, my approach to the management of type 2 diabetes has become more nuanced, tailoring therapy for each patient, rather than “one size fits all”. After lifestyle and metformin, the choice of a 2^nd line agent should be based on the:

a)  Amount of A1C lowering desired

If the desired A1C lowering exceeds the demonstrated ability of an agent to achieve, then it should not be used. For example, a DPP-4 inhibitor may be a reasonable choice for an A1C between 7.0 – 8.5% (A1C lowering ~ 1%), but would not be a good choice if the A1C exceeded this range. If the desired A1C lowering exceeds 1.0 – 1.5% and hypoglycemia or weight gain is not of particular concern, a sulfonylurea or even pioglitazone (in selected patients) may be more effective.

b)  Potential for side effects

If weight gain or hypoglycemia is of concern, then an incretin agent would be advantageous over a sulfonylurea, such as glyburide. If weight loss is desired, then only the injectable incretin mimetics have been demonstrated to achieve this. If the relative lack of data regarding possible long-term side effects is concerning, then using more established agents may be more appropriate until more long-term data is available.

c)   Cost

Before initiating any new agent, it is important to establish whether the patient has extended (private) medical coverage. If no extended medical coverage is available to help defray the higher cost of these new agents, then less expensive agents may be satisfactory, unless side effects preclude their use.

Type 2 diabetes is a complex metabolic condition with many variables influencing its presentation, progression, risk of complications and metabolic control. The more therapeutic options available, the more challenging it can be for prescribers to choose the right therapy. Incretin agents offer additional options to address some of this complexity and improve the ability to tailor therapy for individual patients. If used properly, in the right patient, under the right circumstance, incretin agents can improve glycemic control and offer additional benefits, while avoiding some common side effects of more traditional agents.

References (Note: Article requests require a login ID with CPSBC or UBC)

1. Canadian Diabetes Association 2008 Clinical Practice Guidelines for the prevention and management of diabetes in Canada. Pharmacologic management of type 2 diabetes. Canadian Journal of Diabetes 2008; 32(1): S53 – S61. (View article)
2. Lago RM, Singh PP, Nesto RW. Congestive heart failure and cardiovascular death in patients with prediabetes and type 2 diabetes given thiazolidinediones: a meta-analysis of randomised clinical trials. Lancet 2007 Sep; 370: 1129-36 (View article with CPSBC or UBC)
3. Drucker DJ, Nauck MA. The incretin system: glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors in type 2 diabetes. Lancet. 2006; 368: 1696-705. (View article with CPSBC or UBC)
4. Amori RE, Lau J, Pittas AG. Efficacy and safety of incretin therapy in type 2 diabetes: systematic review and meta-analysis. JAMA 2007; 298: 194-206. (View article with CPSBC or UBC)

What I did before

In counseling patients regarding their lipids, where appropriate, I strive to discuss risks and benefits of pharmacologic therapy, including a cardiac risk assessment.  Although I recognize its limitations, the Framingham Risk Score remains central to most guidelines, including the Canadian Cardiovascular Society lipid guidelines.  Given time constraints, especially in my perceived low risk or low-moderate risk patients, I often found myself estimating patient risks instead of actually taking out the scoring tool and adding up the points.

In addition, patients are often resistant to adding yet another medication to their existing regimen.  Occasionally, I’ve had low risk patients who were very keen on taking statins “just in case.”  Hard numbers often help make the decisions in these patient groups.

This app changed my practice

In the Palm Pilot days (a long-discontinued handheld personal digital assistant), I used various Framingham score tools.  With the torrent of apps now available for the iPhone, I looked for an app with direct applicability to Canadian physicians, using SI units and recommendations consistent with the CCS guidelines.  In the last year, the CCS released their mobile lipid guideline app (iPhone/iOS only).

This app allows a very rapid entry of relevant parameters to perform risk assessments using the Framingham Risk Score but also the Reynolds Risk Score (which takes into account family history and hs-CRP, but is for use in non-diabetic patients – more information is available at http://www.reynoldsriskscore.org/).  There is also a calculator to determine if your patient meets criteria for the metabolic syndrome.

As you enter values into the tool, the slider on the bottom moves up to show the 10 year risk for a cardiac event.  In addition, the “Show Treatment Info” tab just above the slide rule pops up the recommended treatment thresholds and targets for the calculated risk.

Other useful aspects of the app include summaries of the actual CCS 2009 lipid guidelines, as well as discussions about the difference between the Framingham and Reynolds risk scores, and information about the CCS’s approach to the metabolic syndrome.

The CCS 2009 Lipid Guideline apps is available for free from the iTunes App store.

http://itunes.apple.com/ca/app/ccs-lipid-guidelines/id394804422?mt=8&uo=4

What I do now

Because of the simplicity and speed of data entry, I now use this app whenever I need to perform a risk cardiac assessment on a patient.  Not surprisingly, I found that my own estimations were often incorrect (both over- and under-estimating), and this tool provides a convenient check against my own assumptions.

Whether or not you choose to apply the CCS guidelines, or accept the validity of the metabolic syndrome is beyond the scope of this article, but I have found the scores generated by the app greatly help in patient decisions.  The moving slider on the bottom is quite illustrative for patients, and the pop-up windows showing treatment thresholds and targets has helped me convince patients to either start or, in some cases, not take, lipid lowering therapies.

We need more tools that help apply guidelines and current evidence, in a user-friendly and efficient manner.  The CCS lipid app is a great illustration of this.

You can see the other CCS apps at this link (note: as of Jan 2012, the CCS does not make any Android apps):

http://www.ccs.ca/guidelines/mobile_apps_e.aspx

References

1. CCS 2009 Lipid guidelines (pdf download) http://www.ccs.ca/download/consensus_conference/consensus_conference_archives/2009_Dyslipidemia-Guidelines.pdf
2. CCS mobile apps http://www.ccs.ca/guidelines/mobile_apps_e.aspx
3. Reynolds Risk score http://www.reynoldsriskscore.org/faq.aspx

As 2011 draws to a close, I’d like to take an opportunity to thank all of our readers for their support, suggestions, and encouragement.  It’s been a very gratifying experience for all of us involved at This Changed My Practice.

To our authors: thank you for your enthusiastic responses to article and topic requests as well as the replies you’ve offered our readers in the comments section.

I’d also like to take some time to thank our editorial support team: Drs. Bob Bluman, Christie Newton, Daniel Ngui, and Shirley Sze.  Also, we wouldn’t be able to bring these to you without the amazing efforts of Ms. Nina Zoric, our Educational Program Coordinator at UBC CPD.

When we first launched the site, one of the guiding principals was to build a site that would draw interactivity and feedback from physicians and encourage a dialogue between readers and authors, but also readers to each other.  You didn’t disappoint: I’m proud to say that our site seems to attract more written comments and dialogue than most other, much larger medical sites and this is a testament to your active participation.

Your votes help shape discussion and this past year, 76% of the time readers stated they would “likely” or “definitely” change their practice after reading one of our articles.

This year’s top 5 articles for concurrence (with scores of >90% for “likely” or “definitely” change practice) were:

1. Monitoring of cardiovascular disease risk in people with chronic mental illness

2. The outcomes of prematurity

3. Don’t Request Testosterone Levels for Women’s Low Sexual Desire

4. Advocating Fallopian Tube removal at the time of hysterectomy to prevent ovarian cancer

5. Management of maternal thyroid disease in pregnancy

In the coming year, watch for more features aimed at enhancing our local British Columbia – specific CPD needs. Where applicable, we’ll strive to post (alongside the main article) relevant BC Guidelines, billing tips or local initiatives and resources.  This doesn’t alter our original mission: topic articles will still be independent of any guidelines and remain the author’s statement of change.  At times, there may be disagreement with guidelines, but I’ve always maintained that this encourages debate and reflection, one of the main reasons for our site’s existence.

You can also review our main website features at this link:

http://thischangedmypractice.com/key-site-features/

On behalf of all of us at This Changed My Practice, I’d like to wish you and your families a healthy, happy holiday season.

Steve Wong, MD, FRCPC

Internal Medicine

Clinical Assistant Professor, Department of Medicine, UBC

Medical Director, Clinical Practice Reviews, UBC CPD

Medical Director, This Changed My Practice, UBC CPD

www.thischangedmypractice.com – Practice changing evidence and tips

PLEASE NOTE:

NO CREDITS ARE GIVEN FOR THIS POSTING

What I did before

Every year, one-third of older adults (age greater than 65) experience one or more falls.¹  One therapy with the potential to reduce both falling and fractures is vitamin D supplementation, possibly due to a direct stimulation of vitamin D receptors on muscle tissue.²  Often the patients that would most benefit from vitamin D (frail older adults with frequent falls) have swallowing issues that make swallowing large vitamin pills difficult.  Since “there is no correct dose” and it is “only a vitamin” I often administered larger doses (such as yearly courses of 50 000 IU cholecalciferol once per week X 8 weeks) to make administration easier for patients with swallowing issues.

What changed my practice

Unfortunately, a closer look at the issue revealed the appropriate dose of vitamin D necessary to safely reduce fall and fracture risk remains controversial.  A recent meta-analysis of all studies done to date³ demonstrated that “high dose” vitamin D reduced falls by 23 percent (RR 0.77, 95% confidence interval 0.71 to 0.92) when “high dose” was defined as 700 to 1000 IU per day.  Lower doses (less than 700 IU) had no effect on fall risk.  The effects of doses higher than 1000 IU had not been examined previously to the publication of this meta-analysis.  It is also important to remember that large doses of vitamins are not necessarily benign; the increase in mortality with high-dosage vitamin E⁴ should serve as a cautionary example.

After the publication of the above meta-analysis, a randomized, controlled, double blind study⁵ examined the effect of a massive yearly doses of vitamin D on falls and fractures.  The investigators recruited a large number of older adult women (median age of 76 years, n=2258) that were at high risk for falls (defined as the subject being a self-reported faller, having a previous fracture, or having a family history of maternal hip fracture).  The study intervention was 500 000 IU cholecalciferol given as 10 tablets taken on a single day.  Unfortunately, the large-dose vitamin D group both fell and had more fractures than the placebo group.  In fact, there was approximately one more fracture per 100 person-years in the vitamin D group as compared to the placebo group. Of even more concern, fracture rates in the treatment group were highest in the first 3 months following the large dose of vitamin D, suggesting a direct toxic effect.

What I do now

There is support for using vitamin D to prevent falls in older adults, but only in a dose ranging from 700 IU to 1000 IU per day.  I no longer give patients larger doses of vitamin D at less frequent intervals; in fact this practice might have been causing harm. There is no literature to determine what the impact of a more temperate but larger dose of vitamin D will have on fall and fracture rates.  Like any other medication, large doses of vitamins can be harmful.

References: (Note: Article requests require a login ID with CPSBC or UBC)

1. Tinetti ME, Speechley M, Ginter SF. Risk factors for falls among elderly persons living in the community. N Engl J Med 1988;319:1701-7. (View article with CPSBC or UBC)
2. Bischoff-Ferrari HA, Borchers M, Gudat F, Durmuller U, Stahelin HB, Dick W. Vitamin D receptor expression in human muscle tissue decreases with age. J Bone Miner Res 2004;19:265-9. (View article with CPSBC or UBC)
3. Bischoff-Ferrari HA, Dawson-Hughes B, Staehelin HB, et al. Fall prevention with supplemental and active forms of vitamin D: a meta-analysis of randomised controlled trials. BMJ 2009;339:b3692. (View article with CPSBC or UBC)
4. Miller ER, 3rd, Pastor-Barriuso R, Dalal D, Riemersma RA, Appel LJ, Guallar E. Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality. Ann Intern Med 2005;142:37-46. (View article with CPSBC or UBC)
5. Sanders KM, Stuart AL, Williamson EJ, et al. Annual high-dose oral vitamin D and falls and fractures in older women: a randomized controlled trial. JAMA 2010;303:1815-22. (View article with CPSBC or UBC)

Notes from the BC Guidelines

http://www.bcguidelines.ca/guideline_vitamind.html

There is good evidence that supplementation with at least 800 international units (IU) of vitamin D₃ per day, combined with calcium, is required to reduce the risk of fragility fractures, therefore 800 – 1000 IU daily is recommended (although the optimum daily requirement of vitamin D₃ is not known).^4,5,6 Weekly dosing (one week’s adult dose of vitamin D₃ taken as a single weekly dose, i.e. 7000 IU) or monthly dosing (one month’s adult dose of vitamin D₃ taken once a month, i.e. 30,000 IU) may be more convenient for some patients and has been shown to be safe.^1,4,7 At this time, high doses of vitamin D₃ once a year is not recommended as recent evidence has shown possible increased fracture risk.⁸

Population at Risk

The BC population is at risk of low vitamin D levels from autumn to spring. There is no clinical utility in performing vitamin D tests on patients who are thought to be at risk for sub-optimal vitamin D levels and who would benefit from vitamin D supplementation.

Vitamin D Supplementation without Testing

Because vitamin D supplementation in the general adult population is safe, it is reasonable to advise supplementation without testing. Routine testing of vitamin D levels [25-hydroxyvitamin D or 25(OH)D] is not medically necessary prior to or after starting vitamin D supplementation.

Utilization and Cost of Serum Vitamin D Testing in BC

Utilization of vitamin D testing [as 25(OH)D] in BC has increased ten-fold in the past five years. Medical Service Plan expenditures are approximately $3 million annually for outpatient vitamin D testing with a cost per test of $93.63 in 2009.

What I did before

Upper respiratory infections are the most common illnesses seen in childhood, and the symptoms are often disruptive for both the child and the whole family.  Parents are highly desirous of relieving symptoms of cough and congestion, particularly at night when these interfere significantly with sleep. Recent studies and guidelines have raised serious concerns about the safety and benefit of OTC preparations such as dextrometorphan and oral decongestant/antihistamine preparations, and it is recommended these no longer be given to children.  We are therefore left with little to offer except buckwheat honey (1) – until this study.

What changed my practice

A study was published in December 2010 (1) which determined the value of a single application of vapor rub or petrolatum at bedtime to the neck and chest to reduce nocturnal cough, congestion and to improve sleep. Vapor rub is a topical preparation containing camphor, menthol and eucalyptus oil and has been in use for over 150 years.  138 children ages 2 to 11 were recruited, and divided into groups to receive a single application of vapor rub, petrolatum or no treatment.  As vapor rub has a very characteristic aroma, parents were partly blinded to the test substance by applying the vapor rub to their own upper lip and nostrils before applying it to the child (in clinical practice vapor rub should NOT be applied to the lip or nose, but only the upper chest and neck). Surveys were administered to parents on 2 consecutive nights – on the day of presentation with no medication the previous evening, and on the next day when vapor rub, petrolatum or no treatment had been applied to their child’s chest and neck before bedtime.  Between treatment groups, significant differences in improvement were detected in cough severity, congestion and sleep difficulty with vapor rub scoring the best and no treatment the worst.  Sleep improved significantly for both the child and (not surprisingly) the parents.

What I do now

I inform parents that OTC oral medications for cough and cold symptoms are not advised, but that an application of vapor rub applied to the neck and chest may be helpful in relieving cough and improving sleep.  There is also some evidence that a single dose of honey (2) at bedtime may be a helpful addition to the cough and sniffle armamentarium.  So much for sneering at an old folk remedy.

References

1)  Paul IM, et al, Vapor Rub, Petrolatum, and No Treatment for Children With Nocturnal Cough and Cold Symptoms, Pediatrics 2010;126;1092 http://pediatrics.aappublications.org/content/126/6/1092

2)  Paul IM, et al, Effect of honey, dextromethorphan, and no treatment on nocturnal cough and sleep quality for coughing children and their parents,  Arch Pediatr Adolesc Med – 01-DEC-2007; 161(12): 1140-6 http://www.ncbi.nlm.nih.gov/pubmed/18056558

What I did before

In the area of Non-Suicidal Self Injury, I had little knowledge to classify or deal effectively with this type of behaviour in patient encounters.  Often times, these patients would be labelled as Borderline Personality Disorders and with this particular diagnoses, there was generally a lack of treatment options for them.  Patients that exhibit this type of behaviour would often have repeated presentations of self injury that raised uncomfortable feelings in me as a family physicians due to gaps in understanding and knowledge about the condition.  This lack of understanding of this type of behaviour allowed me to treat these patients only by being empathetic and dealing with their wounds.

What changed my practice

We had a presentation by Dr. Lyn MacBeath, one of our local psychiatrists on this topic which improved my knowledge of this condition especially from the patient’s perspective.  I now recognize the inherent high risk of successful suicide (10%) in this population and the need to address non-suicidal self injury with the seriousness that it deserves.  Dr. MacBeath has provided clinicians with guidelines to deal with patients that present with non-suicidal self-injury as well as hand-outs for patients.  These are attached.

What I do now

I am certainly more aware of the increased risk for suicide in these patients and would make a point of asking about suicidality and following through with a Mental Health Assessment, appropriate treatment and referral for resources in mental health +/- addiction services.

I am also more aware that for a lot of these patients that they have problems verbally expressing some very difficult feelings and that often times, they are highly intelligent and artistic and assisting them in finding ways to verbally communicate effectively may eventually help them in their abstinence from self injury.  The twelve step program for addictions seem to be an effective method.

Additional materials:

Download Dr. Lyn MacBeath’s guidelines (View)

Download the patient information sheet (View)

References for the 10 % suicidal risk

Stanley, B, Gameroff, MJ, Michalsen, V, Man, JJ. (2001). Are suicide attempters who self-mutilate a unique population? Am J Psychiatry, 158, 427-432. (View)(UBC Link)

What I did before

Prior to working at a Sleep Clinic, I regularly enquired about patients’ sleep in my psychiatric practice.  I would ask how many hours they slept, and whether they had trouble falling asleep (initial insomnia), staying asleep (middle insomnia) or waking up too early and unable to return to sleep (terminal insomnia or early morning awakening).  The timing in the night of the sleep difficulties can help in differentiating different psychiatric disorders from one another rand from primary insomnia.  I also asked whether patients napped in the day.  Then I would bombard them with a vast array of sedative hypnotics, sedating antidepressants, anticonulsants, or in a fit of desperation, antipsychotics.  Alas, the sleep complaints, often perplexing, persisted.  I had failed to ask the most important question when assessing insomnia concerns in patients with or without a primary psychiatric disorder: How long do you spend in bed?

What changed my practice

Asking that simple question  revealed that many patients with insomnia complaints spend inordinate amounts of time in bed (TIB to us “sleep people”).  Working at a sleep clinic, I also learned that generally we are all poor estimators of sleep, usually underestimating our total sleep time (TST).  When patients develop insomnia, they commonly resort to increasing their TIB, which only increases sleep fragmentation.  Then they lie down and nap in the day, also increasing sleep fragmentation at night.  The treatment is not to add increasing dosages and combinations of sedating medications.  Even patients with primary psychiatric disorders that have a biologic basis for secondary insomnia and adopt poor sleep habits can benefit from behavioural interventions for improving sleep.

What I do now

So now when I assess patients with insomnia complaints, both at the sleep clinic, and in my psychiatric practice, they complete a sleep diary documenting both TIB and estimated TST.  TIB should approximate TST to produce good sleep efficiency (SE).  Therefore if patients “guess” they sleep only 6 hours at night, but have taken to spending upwards of 9-12 hours in bed (often with napping!), they are instructed to decrease the TIB to match the estimated TST (ie 6 hours in bed) for 3 weeks (and no lying down or napping in the day!).  This usually improves the SE, and they report sleeping most of their allotted TIB.  Then they can gradually increase the TIB by 15 minutes a night per week as long as good SE is maintained.  This way the patients discover what their individual optimal TIB will be that allows them to fall asleep and stay asleep throughout the night.  If the SE does not improve after the 3 week intervention, especially in the absences of a primary psychiatric disorder, a referral to a Sleep Disorder Programme is in order.

So before resorting to sedative hypnotic, antidepressant and/or antipsychotic polypharmacy for complaints of insomnia, don’t forget to ask: How long do you spend in bed?  You may be astounded by the answers and your ability to intervene, without the immediate use of medications.

Recommended reading:

“Say Goodnight to Insomnia” by Gregg Jacobs, Publisher: Owl Books

What care gaps have been identified?

Patients with advanced cancer are faced with disease that cannot be cured.  Treatment considerations include ‘active’ disease-directed therapy aimed to slow tumour growth, symptom management and palliative or supportive care.   Oncologists often view their primary goal as improving survival and, hence, directing active therapy.  Unfortunately, the transition from a focus on active, disease-directed treatment to palliative care often occurs late, commonly within just days to weeks of the end of life.  Honest and candid conversations about prognosis and establishing goals of care can be difficult and as a consequence may be delayed, which can hinder access to quality palliative care for the patient and support for their caregivers.  Analysis of patterns of care suggests that patients are increasingly receiving chemotherapy and requiring more frequent visits to the hospital and emergency department in the last 2 weeks of life, and are often referred to hospice only in the very last days of life. (1)

Data that answers these gaps

In a recent randomized trial published in the New England Journal of Medicine, patients with advanced lung cancer who received both chemotherapy and also received care and support from a palliative care team immediately after their diagnosis lived almost three months longer than those who received chemotherapy alone. (2)   Improved patient-MD communication has been associated with a better understanding of prognosis, a greater likelihood of seeking hospice care and reduced likelihood of pursuing futile therapy before death.(3)  In addition, as reported in another related study in the Journal of Clinical Oncology, caregivers of patients with advanced, terminal disease who receive palliative therapy experience less emotional stress (4).

What recommendations are suggested?

The American Society of Clinical Oncology recently published a guidance to direct individualized care for patients with advanced cancer.(5)   This statement advocates for candid discussions which provide disease-directed and supportive care options for patients with advanced cancer throughout the continuum of care.  While patients may wish to pursue any possible anticancer treatment even in the last weeks of life, such decisions need to be informed with a realistic assessment of prognosis and limitations of treatment.   In individualized circumstances, consideration may be given to participation in clinical trials; however it is important to ensure that such participation is aligned with a patient’s personal goals and preferences.  When no reasonable therapeutic options exist, patients should be encouraged to transition to palliative care to maximize their quality of life.  Beyond providing cancer-directed therapies, it is the responsibility of the care provider team (including oncologists and GPs) to restrain from the use of ineffective therapies and to ensure that patients are given the opportunity to benefit from palliative care through the course of their illness and to spend their final days with dignity and peace of mind.

References: You can request articles from CPSBC https://www.cpsbc.ca/library/library-article-requests or log in with your UBC ID.

1. Earle CC, Landrum MB, Souza JM, et al: Aggressiveness of cancer care near the end of life: is it a quality-of-care issue?  J Clin Oncol 26:3860-3866, 2008 (View article)
2. Temel JS, Greer JA, Muzikansky A, et al: Early palliative care for patients with metastatic non small-cell lung cancer. N Eng J Med 363: 733-742, 2010 (View article )
3. Robinson TM, Alexander SC, Hays M, etal: Patient-oncologist communication in advanced cancer: Predictors of patient perception of prognosis.  Support Care Cancer 16:1049-1057, 2008 (View article with UBC)
4. Wright AA, Keating NL, Balboni TA, et al: Place of death: Correlations with quality of life of patients with cancer and predictors of bereaved caregivers’ mental health. J Clin Oncol 28:4457-4464, 2010 (View article )
5. Peppercorn JM, Smith TJ, Helft PR etal: American Society of Clinical Oncology Statement: Toward Individualized Care for Patients with Advanced Cancer. J Clin Oncol 29:755-760, 2011 (View article with UBC)

Useful link: 

Practice Support Program End of Life module (PSP EOL module)

http://www.gpscbc.ca/psp/learning

What care gaps I noticed

Nasal woes can cause lots of complications. Most of them start insidiously but can progress steadily.  Awareness by the family physician of what “can happen” is very important.  Most important is the fact that even though a patient doesn’t complain of nasal congestion symptoms, they sometimes are severely affected by nasal mucosal swelling and often times have had problems for many years undetected.

What changed my practice

After years of examining an awful lot of noses, I came to realize that direct visualization of the nose is the best method in conjunction with a good history to help dissect the patient’s problem.  One without the other will result in a missed diagnosis.  Most persistent symptoms are under appreciated by the patient until they cause a complication.  Remember, the patient doesn’t have to complain of nasal congestion in order to have a significant problem with nasal mucosal swelling.

Most commonly, if they have a septal deviation to severe enough degree, then they may never get nasal congestion symptoms even though they have marked nasal mucosal swelling.  On the other hand, the patient may have a very large nasal passage opening and can then “tolerate” much more mucosal swelling before actually causing some degree of obstruction.  These patients will deny that they have any nasal congestion symptoms when asked even though they have significant pathology.  In those cases,  they may only complain of a runny nose, that is either runny down the front and dripping like a tap or running down the back of the throat and presenting with lots  of “mucous in the back of my throat” or persistent throat clearing .  The latter of which usually causes great distress for all others around them because of the repetitive irritating nature of it and oftentimes the patient doesn’t even realize there is a problem.

The converse is true for patients with very small nasal passages who obstruct very early with sometimes very little mucosal swelling.  Petite “ski jumped” shaped noses are fashionably beautiful but can cause severe distress very early for their owners.  The bigger the nose and the wider the nasal openings, the less trouble the patient will have with nasal congestion symptoms.  Upon presentation to the office, these “petite” nose patients may have little to show physically for their symptoms at the time of examination but are severely obstructed at other times in the day especially in the evening.  A little bit of mucosal swelling in these patients can cause severe obstruction much earlier.

Nasal congestion symptoms are usually worse at night when patients lie down to go to sleep or early in the morning.  During the day patient symptoms are sometimes at their best and that, unfortunately, is usually when their noses are examined by their doctor. The history from your patient can be very important in conjunction with the physical examination.

What I recommend, practice tip

I have compiled a list of some of the signs and symptoms to watch for in the presenting patient with allergic rhinitis which I hope you find useful.

Symptoms: stuffy nose, sore throat especially at night or first thing in the morning, snoring, bad breath, itchy nose, crusty nose, ear plugging, fluctuating hearing, dry or itchy eyes, and nose bleeds (sometimes this can occur for two years before they develop signs of nasal congestion).

Complications are interference with sleep and subsequent effects on cognition, irritability and difficulty concentrating, and sometimes “brain fog”.  There could be recurrent infections – sinus, ear or recurrent sore throats with negative cultures.

More long term complications include gingival and periodontal disease.  In children, oral facial malformation with open bites can develop.  It can also affect a patient’s ability to perform as well as they should otherwise be doing.  In other words, the nose can cause a significant effect on the overall quality of life.  Not a bad list considering it is “just a stuffy nose!”

A final thought to leave you with from one of my old professors: Remember, the nose is that part of the respiratory track that is easily accessible by your finger and otoscope!  So most importantly, get use to looking at lots of noses as a routine part of your physical exam.  You will more easily pick up the pale boggy turbinates sometimes with lateral wall pseudo turbinates that are most commonly seen in the allergic nose — even in infants as young as six months of age.  It will make you a better clinician and your patients will love you even more when you use this information to help sort out the true ramifications of “just a stuffy nose”!

Additional reading:

http://www.entusa.com/nose_photos.htm

What I did before

In 2003 a 39 year old male crane operator with a history of a severe crush injury to the left upper limb came to me for treatment of profound allodynia and hyperalgesia (among other symptoms) that had spread from his injury site to all four limbs. He had been diagnosed with Chronic Regional Pain Syndrome and had undergone treatment attempts of all types for years. He was on high dose, long acting oxycodone 20 mg 6 tablets tid = 360 mg/d (morphine equivalent of approximately 540 mg/d). To try to get analgesic control (pain rating 10/10), and eliminate pill burden I rotated the oxycodone to fentanyl. Ultimately he required fentanyl 50 + 25 mcg patches every 3 days (morphine equivalent of approximately 150 mg/d) plus short acting oxycodone 5 mg qid prn for breakthrough (morphine equivalent of 30 mg/d).  Not only did his pain drop down to a rating of only 1-2/10, the signs and symptoms of hyperalgesia and allodynia vanished. In just three weeks he went back to work. This perplexed me so I began searching the literature.

What changed my practice

I found the review article by J. Mao listed below and some other related studies that described Opioid Induced Pain Sensitivity (OIPS), which likely played a key role in the pain presentation of the worker described. Basically, some people manifest symptoms of diffuse spreading pain along with signs of allodynia and hyperalgesia when exposed to high doses of opioids (usually above 3-4 gm/d morphine equivalent, but it can happen at lower doses). The article reviews various lines of evidence, proposes mechanisms and treatments for this condition.

Treatments for OIPS can include opioid rotation or opioid lowering – both of which occurred in the worker reviewed above (ie. 540 -180 = 360 mg drop in the daily morphine equivalent dose, and opioid rotation from oxycodone to fentanyl). Some patients need to come right off the opioid for at least 2-4 weeks to see a change in signs and symptoms. Using an NMDA antagonist like ketamine or dextromethorphan when initiating an opioid can be helpful in preventing OIPS (though the latter two medications have issues of their own and I rarely use them). Methadone is an NMDA receptor antagonist through one of its isomers, the other isomer being a strong Mu opioid receptor agonist. Thus methadone (and to some extent buprenorphine) is a great choice for neuropathic pain patients where OIPS may be playing a role. Care is needed with the conversion between opioids, especially methadone or buprenorphine, since the NMDA glutamate system is involved in both the development of tolerance and OIPS, and conversion doses do not rise linearly. A good reference for conversions is listed below.

What I do now
OIPS is now something I consider whenever I see a patient with allodynia and hyperalgesia, whereas prior I may have simply tried to increase the opioid dose (which would help if tolerance alone was present). I’ve now taken many patients off opioids altogether or done one of the other maneuvers mentioned above and had both signs and symptoms clear. Also, I have found this to be true for some patients who were taking just moderate doses of opioids, far lower than the studies indicate, as with the crane operator above. Thus it is worth considering OIPS in the differential diagnosis when pain appears to be spreading, especially when features of allodynia and hyperalgesia are present.

References: (Note: Article requests require a login ID with CPSBC or UBC)

1. Mao J. Opioid induced pain sensitivity: Implications in clinical opioid therapy. Pain 2002;100:213-217. (View article with CPSBC or UBC)
2. McPherson, M.L. Demystifying opioid conversion calculations: A guide for effective dosing. American Society of Health-System Pharmacists, Bethesda, MD, 2009. (book: Woodward library, call number: QV89 .M478 2010)

There are five new pieces of evidence that changed my practice in management and treatment of pneumonia.

Community acquired pneumonia caused by Streptococcus Pneumonia is the 6^th leading culprit of death due to infection in North America.

In the 80’s, first time resistance of Streptococcus pneumonia to Penicillin was noted in South Africa; shortly after it spread widely throughout the world, and currently it has turned into a variably sensitive, intermediate and highly resistant strain.

What changed my practice

In the 90’s, the British Thoracic Society and American Thoracic Society gathered and developed a practice guideline, which was revisited later in the late 90’s and once again in 2007 by the Infectious Diseases Society of America.  By walking through guidelines derived over 10 years, there are 5 major evidences that changed my way of managing community acquired pneumonia.

What I do now

1)    A quick way to assess patients for where, what and when to treat and investigate was brought into practice by the CURB-65 Severity Score for Community Acquired Pneumonia. This method has more practical utility than the pneumonia severity index (PSI) previously used.

Management is guided by the score:

http://www.mdcalc.com/curb-65-severity-score-community-acquired-pneumonia

2)    Penicillin and Amoxicillin came back to Guidelines treatment of mild to moderate pneumonia due to their preserved ability to eradicate Streptococcus pneumonia in 65% of the cases. They have replaced macrolides and quinolones which previously were first choices, thus the majority of community acquired pneumonia with an intensity of mild to moderate could be easily treated with Amoxicillin +/- Doxycyciline. ^{1, 2, 3, 5}

3)    I also learned to take into consideration the numbers of co-morbidities as an important independent risk factor for severity of pneumonia presentation rather than just looking at patients’ vitals and microbiology reports. The number of co-morbidities is linearly associated with worse outcome due to poor immune response and higher rate of colonization with resistant bacteria. ²

4)    The time to initiation of antibiotics is crucial to improve the outcome in moderate to severe pneumonia. Based on the evidence, antibiotic initiation within the first 6 hours is substantial to successful outcome as the delay will increase the mortality of severe sepsis by 7.8% per hour thereafter. ^{2, 4}

5)    I continue to stay current with the recommendations within the practice guidelines. The outcome of patients in the centers that consistently adopted the practice guideline recommendations has been more favorable in the past 10 years. ²

I hope this brief note can change your practice management in treatment of community acquired pneumonia as well.

References: (Note: Article requests require a login ID with the BC College of Physicians website)

1. Donald E. Low, Joyce de Azavedo, et al. Antimicrobial Resistance among Clinical Isolates of Streptococcus pneumoniae in Canada during 2000, Antimicrobial Agents and Chemotherapy, May 2002, p. 1295–1301 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC127188/pdf/0963.pdf  (View article with UBC)
2. Lionel A. Mandell, Richard G. Wunderink, et al. Infectious Diseases Society of America/American Thoracic Society Consensus Guidelines on the Management of Community-Acquired Pneumonia in Adults, Clinical Infectious Diseases 2007; 44:S27–72 (Suppl 2) (View article with CPSBC or UBC)
3. M. Winters, D.M. Patrick, et al. Epidemiology of Invasive Pneumococcal Disease in BC during the Introduction of Conjugated Pneumococcal Vaccine, Canadian Journal of Public Health, January/February 2008, Vol. 99, No. 1 (View article with CPSBC or UBC)
4. Anand Kumar, Cameron Haery, et al. The Duration of Hypotension before the Initiation of Antibiotic Treatment Is a Critical Determinant of Survival in a Murine Model of Escherichia coli Septic Shock: Association with Serum Lactate and Inflammatory Cytokine Levels. The Journal of Infectious Diseases 2006; 193:251–8 (View article with CPSBC or UBC)
5. Anand Kumar, Ryan Zarychanski, et al. Early combination antibiotic therapy yields improved survival compared to monotherapy in septic shock: A propensity-matched analysis. Crit Care Med 2010 Vol. 38, No. 9 (View article with CPSBC or UBC)

Recommended reading:

Slides for data for susceptibility of strep pneumonia in the US and BC

http://www.ubccpd.ca/susceptibility_of_strep_pneumonia.htm

What care gaps or frequently asked questions have you noticed in the management of this condition?

We receive many referrals for assessment and treatment of women with low sexual desire and ‘low serum testosterone levels’. Although men with repeatedly low serum testosterone levels typically have low sexual desire, no such link has been identified in women. Women’s testosterone production does decrease with age – the component derived from peripheral conversion of adrenal (and ovarian) precursor hormones, most notably DHEA, declines by some two-thirds by ages 60 to 70, and testosterone production from post-menopausal ovaries is highly variable (zero after surgical menopause). Given a lessening of women’s sexual desire with age is reported in most studies, it had been assumed that when testosterone assays accurate at the lower ranges found in women became available, a link between low testosterone and low sexual desire might be identified. When peripheral intracellular production of testosterone from DHEA could be measured, such a link might be even more obvious.

Data that answers these questions or gaps

Now published is a study of 245 women, carefully assessed by extensive structured interview as well as standard questionnaires with and without hypoactive sexual desire disorder (HSDD)[1]. Using “gold standard” assays – i.e. mass spectrometry methods no group difference was found in serum testosterone. Moreover, serum androgen metabolites (a measure of intracellular testosterone as well as ovarian testosterone), also measured by mass spectrometry methods was similar in both groups. Additionally, there are now three prospective studies of prophylactic bilateral salpingo oophorectomy (BSO) at the time of hysterectomy needed for benign disease in perimenopausal women. None of the women receiving elective BSO (plus hysterectomy) acquired sexual dysfunction in the subsequent three to five years[2][3][4]. As well, epidemiological studies of prevalence of HSDD in menopausal women show that although distress about having low sexual desire is increased in surgically menopausal women, the prevalence of low sexual desire per se is not increased compared to naturally menopausal women of the same age[5].

What do you recommend (practice tips) to GPs in managing this problem?

It is recommended not to request serum testosterone levels in women looking for low levels:

1)      Clinically available assays are not accurate at the low levels found in women

2)      Intracellular testosterone is not measured by serum levels of testosterone

3)      There is no evidence that low testosterone is linked to low desire when accurate testosterone assessment (including that made within the peripheral cells) is used.

This recent research shows that supplementing testosterone off-label to women with low sexual desire is not scientifically based and is still recommended against by the American Endocrine Society[6] in part due to absence of long-term safety/efficacy data. For review of (investigational) t-therapy in women see Basson R. Testosterone Therapy for Reduced Sexual Libido in Women. Ther Adv Endocrinol Metab 1(4):155-164, 2010[7].

Reassuring women that “hormonal imbalance” is not proven to be a likely cause of low sexual desire allows them to focus on the known correlates i.e. mood especially depression, sexual self-image, feelings for the partner[8][9][10] and the presence of any sexual dysfunction in the woman herself e.g. dyspareunia or dysfunction in the partner, especially erectile dysfunction in a male partner[11].

References: (Note: Article requests require a login ID with CPSBC or UBC)

Editor’s note: The use of smartphones and mobile, handheld computing devices like the iPhone, iPod Touch and others among physicians is remarkable.  In 2011, 81% of US physicians own a mobile device¹, 54% of physicians access medical information on their smartphone during patient visits².  Currently, the most popular devices are Apple iOS devices (32% iPhone/iPod Touch, 22% Blackberry, 16% Palm, 9% Windows, 4% Android, 2% Symbian¹).

In response to reader requests and the increasing interest in mobile apps, we are launching a series of articles highlighting useful iPhone apps.  These will appear approximately once every three months.

If you have app suggestions, or if you use an Android device and would like to submit an article, please email us at feedback@thischangedmypractice.com.

We hope you enjoy this series of articles.

What I did before

A large part of my practice is focused on the management of diabetes.  A key recommendation from the CDA guidelines is the achievement of A1C targets of 7%.  Also, when appropriate, I encourage patients to perform self-monitoring of blood glucose levels.  I try and teach all my patients what the role of the A1C is as well as how to use their home measurements to guide treatment.

More often than not, patients either don’t test at home at all, or if they do, they test only in the fasting state in the morning, which may give falsely reassuring results as they assume the rest of the day looks similar.

In followup visits, when patients are reviewing their lab results, I often found that patients assumed the A1C is a numeric average of their own glucometer readings (eg. “My A1C is 7.2 – my average glucose must be around 7”).   I advise them that the A1C has a nonlinear correlation with average glucose readings over the last 3 months.   In fact, when I point out to them that an A1C of 7.0% (eg. “at target”) represents an average glucose level of 8.6 mmol/L, many patients respond with surprise and say “wow, that’s actually pretty high.”

These kinds of discussions have been useful in encouraging adherence to therapy and improved understanding of disease pathophysiology, however, I often found myself guesstimating values, which obviously introduces a potential for misleading advice.

This app changed my practice

A free app called Pocket A1C makes it extremely easy to illustrate to patients the relationship between their A1C and average glucose readings.  They can immediately see that I’m not simply making up a number, but more importantly, the real-time, animated sliderule really seems to impact patients when they see me scrolling up and up to get to an A1C of 9.2 as well as see their average glucose of 12 mmol/L.

Get Pocket A1C here (free):

http://itunes.apple.com/ca/app/pocket-a1c/id317041063?mt=8&ign-mpt=uo%3D4

What I do now

I now use Pocket A1C several times a day.  This direct illustration from a lab value (A1C) to a number they may be intimately familiar with (their own glucometer readings) greatly increased patient acceptance of recommendations for intensification of treatment.  I also found the app saved me time in explaining the utility of the A1C assay.

Pocket A1C has helped me achieve targets in patients who may have been reticent to accept more intense treatment and I believe helped me educate my patients more effectively about their diabetes.

References:

1. Manhattan Research
2. SDI’s Mobile and Social Media Study, 2010

What I did before

As most health-care professionals, are well aware, the natural history of Hepatitis C Virus (HCV): can end with cirrhosis and hepatocellular cancer (HCC) as the final outcome. After 20-30 years of chronic HCV infection, anywhere from 20-30% of those with chronic HCV will develop cirrhosis. Once cirrhosis has developed approximately 30% of these will then face the risk of decompensation over the next 5 to 7 years requiring either a life-saving liver transplant or face premature mortality. Once cirrhosis develops in HCV infected patients, the risk of HCC is approximately 3-5% per year which means that after 5 years, the cumulative risk of developing HCC is 15-20%.

British Columbia, unfortunately, has a very heavy burden of HCV. Although the exact prevalence is not known, it is estimated that anywhere from 40-80,000 (or more) residents of BC suffer from chronic HCV and many remain undiagnosed. Across Canada, over a quarter of a million people are estimated to have the infection (1) and the mortality from HCV, based on the premise of no improvements in the current licensed therapy (ie. peginterferon and ribavirin), has been projected to continue to increase.

In BC as in all provinces, HCV dominates the wait-list of those in need of a liver transplant and 35% of all transplants are performed for end-stage liver disease caused by HCV (2).  Although liver transplantation in BC has been associated with an excellent post-transplant survival, the truth remains that there is a tragic discrepancy between the need for transplantation and its availability, as cadaveric organ donation remains the main source of donor organs. The mortality on the wait list, i.e. death from end-stage liver disease before a suitable donor organ becomes available, remains approximately 30% per year (1).

It is very clear to the gastroenterologists/hepatologists at the Vancouver General Hospital (VGH), that to ameliorate the many clinical tragedies associated with treating dying cirrhotic patients, awaiting a life-saving transplant, is to reduce the need for transplantation over the long-term. In this regard, over the past dozen years, we have seen the hepatitis C antiviral agents that we offer our patients, outside of transplantation, evolve and improve.

Hepatitis C is not a homogenous virus.  Although all strains have equal virulence, response to treatment differs amongst the 6 genotypes (G), of which only three (G 1,2 and 3) are common in North America. With genotype 1 (the most common genotype in North America and Europe, and the most frustrating genotype to treat), the likelihood of a sustained virologic response (SVR) has improved from 30% with standard three times a week non-pegylated interferon in combination with ribavirin (3) to 40-50% with pegIFN and ribavirin (4,5).  Patients with G2 and G3 infections have a much greater chance of clearing the virus (approximately 70%) and the duration of therapy is half that of the G1 patients (24 weeks vs. 48 weeks) (4).The combination pegIFN and ribavirin has been the standard in our clinical practice since 2003. For the G1 patients, the difficulty of taking a 48 week therapy with many side-effects, as well as the need to monitor the hematologic profile and thyroid function, is compounded by the fact that the overall odds of achieving a successful outcome is at best, a flip of a coin (in actuality, for those with advanced liver fibrosis and high viral loads, it is far less than a coin toss).

What changed my practice

Until this year, however, there was no other choice open to these patients.  This year, based on the phase III studies, published in the New England Journal of Medicine (6, 7), confirming earlier clinical trials, the American regulatory body, the Food and Drug Administration (FDA) approved the new protease inhibitors, telapravir (7) and boceprevir (6) in combination with pegIFN and ribavirin for patients with HCV G1 infections.  Telapravir (7) for 12 weeks and pegIFN with ribavirin for 24 or 48 weeks, depending on whether or not the HCV disappeared from the blood stream in the early weeks, has a likelihood of HCV sustained clearance of 75%. Similarly, the triple combination of bocepravir, pegIFN and ribavirin for 24-48 weeks, depending on whether early clearance is achieved or not, is associated with a 68% likelihood of sustained clearance (8). Considering that a sustained clearance has been demonstrated to be associated with cure in almost all patients, this is, for health-care professionals and hepatitis C patients alike, a reason for extreme optimism. It should be noted, that the likelihood of a sustained clearance with these new drugs is less in those of African background but this is still far superior than anything that came before.  Although Canadian approval for these new drugs is still pending (as of this writing, July 01, 2011), it is very likely that Health Canada will act similarly to the FDA and allow the same antiviral benefits to Canadians that Americans now enjoy.

What I do now

Although it may seem unusual to write about “changing practice” with drugs that are not yet on the market in Canada, in actuality, myself, and my colleagues at the BC Hepatitis Program at VGH, have been using telapravir since 2007 and boceprevir since 2008 as part of our clinical trials program. We can confirm the outstanding efficacy of these drugs against HCV G1 infection and our patients are very appreciative. We have found the side-effect profile of the new protease inhibitors to be very manageable with the outstanding help of our excellent hepatitis nurses. We no longer offer patients with HCV G1 infections the “standard of therapy” as currently available because we know that it suboptimal and obsolete. We advise our patients to either wait for telapravir or boceprevir to become available (and for the majority, this also means waiting for BC Pharmacare to cover these antiviral agents) or to consider entry into a clinical trial with these agents or similar agents that we are also finding to be efficacious.

Lastly, we have reported that fewer patients infected with HCV G2 (the “easy to treat” genotype) are being sent for transplant assessment because this genotype is amenable to pegIFN and ribavirin therapy (8). This is clear epidemiologic evidence that effective antiviral therapy can decrease the need for liver transplantation and save lives. We expect that telapravir and boceprevir will be able to have the same epidemiologic effect over the long-term for G1 patients. The “future is now” and victory in the war against HCV is finally in sight. For the sake of our patients, it has to be.

References: (Note: Article requests require a login ID with CPSBC or UBC)

1. Sherman M, Shafran S, Burak K et al.  Management of chronic hepatitis C: consensus guidelines.  Can J Gastroenterol 2007; 21 (suppl C): 25C-34C. (View article with CPSBC or UBC)
2. Haque M, Scudamore CH, Steinbrecher UP et al.  Liver transplantation: current status in British Columbia.  BC Med J 2010; 52: 203-10. (View article with CPSBC or UBC)
3. McHutchinson JG, Gordon SC, Schiff ER et al.  Interferon alfa 2b alone or in combination with ribavirin as initial treatment for chronic hepatitis C.  N Engl J Med 1998: 339: 1485-92. (View article with CPSBC or UBC)
4. Hadziyannis SJ, Sette H Jr, Morgan TR et al.  Peginterferon alpha 2a and ribavirin combination therapy in chronic hepatitis C: a randomized study of treatment duration and ribavirin dose.  Ann Intern Med 2004; 140: 346-55. (View article with CPSBC or UBC)
5. McHutchinson JG, Lawitz EJ, Shiffman ML et al.  Peginterferon alpha-2b or alpha-2a with ribavirin for treatment of hepatitis C infection.  N Engl J Med 2009; 361: 580-93. (View article with CPSBC or UBC)
6. Poordad F, McCone J Jr, Bacon BR et al.  Boceprevir for untreated chronic HCV genotype 1 infection.  N Engl J Med 31: 364: 1195-06. (View article with CPSBC or UBC)
7. Jacobson IM, McHutchinson JG, Dusheiko G et al.  Telaprevir for previously untreated chronic hepatitis C virus infection.  N Engl J Med 2011; 364: 2405-16. (View article with CPSBC or UBC)
8. Hashim A, Haque M, Krajden M et al.  Shift in HCV genotype in a liver transplant referral centre over 10 years: the British Columbia experience.  Can J Gastroenterol 2010; 24 (suppl A): 158 A (abstract). (View article with CPSBC or UBC)

What I did before

Clostridium difficile infection (CDI) most commonly arises following antibiotic use in hospitalized patients.  Isolation of suspected cases and hand hygiene are two of the most important means of prevention, but despite our best efforts CDI remains a huge problem.  Even after successful treatment with metronidazole or vancomycin, anywhere from 20-35% of patient will relapse, but the risk factors for relapse differ among studies.  One important risk factor is continuation of other antibiotics, which prevents repopulation of the gut with normal bacteria.  The role of other medications, including proton pump inhibitor (PPIs), has been less clear.  PPIs are very effective at preventing gastrointestinal bleeding in hospitalized patients, and C. difficile spores are acid resistant.  How important are PPIs as a risk factor for initial or recurrent CDI?

What changed my practice

Several recent publications specifically examined the role of acid suppression in CDI.  Most striking was the study by Howell et al¹ that found an incremental increase in the risk of initial CDI with increasing acid suppression (H2 receptor antagonists (H2RA), once-daily PPIs, or more frequent PPIs). A second study by Linsky et al² found that administration of PPIs within 14 days of diagnosis was an independent risk factor for CDI recurrence, with an adjusted HR of 1.42 (higher in elderly patients).  There is also accumulating evidence that PPIs are commonly used in inpatients for indications other than those recommended in published guidelines.

What I do now

PPIs remain the drug of choice for several indications, including treatment of bleeding ulcers or GERD, and stress ulcer prophylaxis in selected high-risk patients.  These include patients on NSAIDs plus anticoagulants, corticosteroids, or a history of NSAID-induced ulcers; patients with severe head or spinal trauma; burn patients; and ICU patients with coagulopathy.  However, PPIs are frequently used for routine ulcer prophylaxis in patients who do not meet these criteria, in the absence of clear evidence of a benefit versus other forms of ulcer prophylaxis (such as H2 blockers) in these settings. Moreover, many patients started on PPIs in hospital are frequently continued on these medications after discharge, even after CDI is diagnosed.

Based on recent literature, my current practice is to carefully consider whether PPIs or H2 blockers are truly indicated in inpatients, and to stop them if they are not.  In patients with CDI infection, I try to discontinue anti-secretory therapy whenever possible. With all prescribed medications, physicians need to carefully consider the potential harm to patients when they write their orders, and be aware of medical evidence that shifts the balance in favor of drug avoidance. While PPIs have a long track record of efficacy and safety, the increasing incidence and severity of CDI may shift the risk/benefit ratio of these drugs.

References: (Note: Article requests require a login ID with CPSBC or UBC)

1. Howell MD, Novack V, Grgurich P, Soulliard D, Novack L, Pencina M, Talmor D. Iatrogenic gastric acid suppression and the risk of nosocomial Clostridium difficile infection. Arch Intern Med. 2010 May 10;170(9):784-90. PubMed PMID: 20458086. (View article with CPSBC or UBC)

2. Linsky A, Gupta K, Lawler EV, Fonda JR, Hermos JA. Proton pump inhibitors and  risk for recurrent Clostridium difficile infection. Arch Intern Med. 2010 May 10;170(9):772-8. (View article with CPSBC or UBC)

What I Did Before

Tight glucose control (reflected in A1C), reduces the risk of microvascular complications, such as retinopathy, nephropathy and neuropathy in patients with diabetes. This relationship holds true even to A1C levels below 7%. Until recently, many assumed that tight glucose control also reduced the risk of cardiovascular disease (CVD) in diabetes. For this reason, in the past, I would target an A1C as low as possible (even below 6.5%) for all my patients with diabetes in order to minimize both microvascular and macrovascular (CVD) complications. However, recent studies suggest that the relationship between glucose control (A1C) and cardiovascular disease is more complex than we may have realized.

What Changed My Practice

The ACCORD and ADVANCE studies were large (>10,000 subjects) multicentre trials, which examined the effect of tighter glucose control on CVD endpoints (nonfatal MI, nonfatal stroke or cardiovascular death) in older type 2 diabetes subjects. Using multiple glucose lowering therapies (including TZDs and insulin), the ACCORD trial achieved an average A1C of 6.4% in the intensively treated group (vs. 7.5% in the standard group). The trial was stopped early, because of a statistical increase in overall death (a secondary outcome) in the intensively treated patients. Most of these deaths appeared to be from cardiovascular causes, but the underlying reason for the increase in mortality was not clear. The ADVANCE study achieved an A1C of 6.5% in the intensive group (vs. 7.3% in the standard group), but did not show a significant difference in overall or cardiovascular mortality. A third, smaller study, VADT, also did not show a difference in CVD or death between the more intensively treated patients (A1C 6.9%) vs. the standard group (A1C 8.4%). There were a number of limitations to each of these studies, but the overall results suggested that tighter glucose control did not seem to reduce CVD events in older patients with established type 2 diabetes. However, a subsequent meta-analysis including these 3 trials, along with UKPDS and PROactive, showed a statistical reduction in MI and cardiovascular death in intensively treated patients, but with no difference in overall mortality. Furthermore, longer-term follow-up of UKPDS patients seemed to show benefit to earlier intensive therapy.

What I Do Now

Based on these results, I now tailor glucose targets more specifically to each patient. It appears that once CVD is established (i.e. older patients with longer duration of diabetes), the benefits of intensive glucose-lowering therapy are not as clear. However, tighter glucose control still seems to improve CVD risk in younger patients with less established disease. For younger patients with no pre-existing CVD or other significant risk factors (hypertension, smoking, family history of CVD), I continue to target an A1C below 7% (especially if it can be easily achieved). However, for older patients (> 50 years), with a longer duration of diabetes (> 15 years), I target an A1C of ~7%, but no lower. This target will avoid the potential downsides of intensive therapy (such as hypoglycemia and possible increased CVD risk), while still providing protection against microvascular disease. Finally, for patients with significant comorbid illness and a limited life expectancy, I target a higher A1C 7.5-8%. In this way, I try to avoid the burden and risk of intensive therapy, if the patient is not likely to see a benefit.

References: (Note: Article requests require a login ID with CPSBC or UBC)

1. The Action to Control Cardiovascular Risk in Diabetes Study Group. Effects of Intensive Glucose Lowering in Type 2 Diabetes. N Engl J Med 2008; 358: 2545-59. (View article with CPSBC or UBC)
2. The ADVANCE Collaborative Group. Intensive Blood Glucose Control and Vascular Outcomes in Patients with Type 2 Diabetes. N Engl J Med 2008; 358:2560-72. (View article with CPSBC or UBC)
3. Duckworth W. Abraira C, Moritz T, et al. Glucose Control and Vascular Complications in Veterans with Type 2 Diabetes. N Engl J Med 2009; 360 (2): 129-39. (View article with CPSBC or UBC)
4. Ray K, Seshasai SR, Wijesuriya S, et al. Eff ect of intensive control of glucose on cardiovascular outcomes and death in patients with diabetes mellitus: a meta-analysis of randomised controlled trials. Lancet 2009; 373: 1765–72. (View article with CPSBC or UBC)

What I did before

When I was in training as a gynecologic surgeon, I was taught how to do a “proper” hysterectomy and “proper” tubal ligation. I practiced until I had mastered it. By surgical convention, when we did a hysterectomy and planned to leave the ovaries in situ (in pre-menopausal women); we left the fallopian tubes inside the patient too.  At the time of tubal ligation, we clipped or burned the tube and left it inside the patient.

What changed my practice

High grade serous cancer of the ovary represents about 2/3rds of the cases of ovarian cancer that we see. These cancers are often diagnosed at an advanced stage.  While this cancer usually responds to initial treatment, it frequently recurs and is not curable in the majority of patients.  A growing body of knowledge reveals that the majority of cases of high grade serous “ovarian” cancer actually are fallopian tube cancers. The precursor lesions begin in the fimbriated end of the fallopian tube and the cancer spreads from there. This knowledge about the true origin of this devastating cancer completely changed my surgical practice.

What I do now

I now advise patients to consent for removal of the fallopian tube at every single hysterectomy.  Family Physicians can advocate for their patients to ensure the fallopian tube is removed at hysterectomy and tubal ligation. My hope is that by removing the fallopian tube we will prevent many cases of this terrible disease. As a gynecologic oncologist, the majority of my patients already have cancer. The potential for a major impact in ovarian cancer prevention rests with general gynecologists—who perform the vast majority of hysterectomies and tubal ligations. Hysterectomy and tubal ligation are among the most common surgeries that a woman will undergo in her lifetime. This September 2010, the Ovarian Cancer Research Program of BC, launched a province-wide educational initiative aimed at every gynecologist in BC.  We are asking gynecologists to remove the fallopian tube at hysterectomy. We are also requesting removal of the fallopian tube at tubal ligation, when a patient requests permanent contraception.  I believe these simple changes in surgical convention hold the promise of preventing future cases of “ovarian cancer”.

For more information:  www.ovcare.ca

References: (Note: Article requests require a login ID with the BC College of Physicians website or with UBC)

1. Przybycin CG, Kurman RJ, Ronnett BM, Shih IM, Vang R.  Are All Pelvic (Nonuterine) Serous Carcinomas of Tubal Origin? Am J Surg Pathol. 2010 2010 October; 34(10): 1407-16. (View article with CPSBC or UBC)

2. Salvador S, Gilks B, Köbel M , Huntsman D, Rosen B, Miller D. The fallopian tube: primary site of most pelvic high-grade serous carcinomas. Int J Gynecol Ca 2009;19:58-64 (View article with CPSBC or UBC)

3. Crum CP, Drapkin R, Miron A, Ince TA, Muto M, Kindelberger DW, et al. The distal fallopian tube: a new model for pelvic serous carcinogenesis. Curr Opin Obstet Gynecol 2007;19(1):3-9. (View article with CPSBC or UBC)

4. Kindelberger DW, Lee Y, Miron A, Hirsch MS, Feltmate C, Medeiros F, et al. Intraepithelial carcinoma of the fimbria and pelvic serous carcinoma: Evidence for a causal relationship. Am J Surg Pathol 2007;31(2):161-9. (View article with CPSBC or UBC)

5. Lee Y, Miron A, Drapkin R, Nucci MR, Medeiros F, Saleemuddin A, et al. A candidate precursor to serous carcinoma that originates in the distal fallopian tube. J Pathol 2007;211(1):26-35. (View article with CPSBC or UBC)

6. Crum CP, Drapkin R, Kindelberger D, Medeiros F, Miron A, Lee Y. Lessons from BRCA: the tubal fimbria emerges as an origin for pelvic serous cancer. Clin Med Res 2007;5(1):35-44. (View article with CPSBC or UBC)

What I did before
I used to buy into the idea that marijuana use was nothing to get too worried about. “It’s a soft drug…. all the kids are doing it… there are few repercussions from using pot”. I didn’t focus too much of my time on marijuana use. Cocaine, heroin, crystal methamphetamine – those were the drugs that needed the attention. If the youth stopped those and continued with marijuana, it seemed to me to be a “safer” choice. I didn’t aggressively target marijuana use from a harm reduction perspective. I’m not sure, looking back, whether I even really asked the questions about how much, how long, and how often used…

What changed my practice
I began consulting to the Provincial Youth Concurrent Disorders Program at BC Children’s hospital. I was seeing youth from 12-25 with anxiety, psychosis, depression, sleep disorder – all in the context of marijuana use.

Through this, I became aware of the high rate of concurrent mental health and substance use disorders in youth (about half of youth with a substance use disorder have a comorbid psychiatric disorder). I discovered that marijuana is one of the top 3 substances used by youth (the others being cigarettes and alcohol), and that early age of onset use is increasing (use as early as 9 years old was 1% in 2003, increasing to 3% in 2008). I learned more about the stages of cognitive development in youth and how substances can affect a developing brain. I learned about the horticulture of marijuana in today’s society and how marijuana may be more potent than in previous years and that THC increase could be associated by a corresponding decrease in cannabidiol, a natural antipsychotic in marijuana (see “Downside of High” on The Nature of Things). Perhaps most persuasively, as a front-line observer, I watched as a functioning youth became more and more psychotic as he smoked large amounts of marijuana every day, and I saw how difficult it was to treat his psychosis even after the marijuana stopped.

What I do now
I no longer think of marijuana as a benign drug. I ask about it every time I see a patient. I counsel harm reduction. I educate about the potential consequences of marijuana use on a developing youth’s brain. I assess for a co-morbid mental health condition. I talk to my kids about drugs (as naturally as I can) with a determined purpose – to warn them and educate them. The longer they can let their brains develop without exposure to drugs, the healthier their brains will be. I encourage early detection of problem marijuana use and referral on for assessment and intervention as a high priority. I aggressively treat it. I don’t want to see potential “wasted” on marijuana.

References:

Smith, A., Stewart D., Peled, M., Poon, C., Saewyc, E. and the McCreary Centre Society (2009). A Picture of Health: Highlights from the 2008 BC Adolescent Health Survey. Vancouver, BC: McCreary Centre Society.

http://www.mcs.bc.ca/pdf/AHS%20IV%20March%2030%20Final.pdf

The Downside of High Documentary directed and written by Bruce Mohun, story-produced by Maureen Palmer, and produced by Sue Ridout for Dreamfilm Productions of Vancouver, The Nature of Things with David Suzuki, 2010.

CBC Documentary: Nature of Things, Down side of high

What I did before

Screening for prostate cancer has been conducted by many general practitioners and most urologists for years without level one evidence supporting its use. Most of the data on which we base our screening practices is indirect and not definitively causally linked to the decrease in mortality that has been observed in prostate cancer in the last 15 years. Critics pointed to the anxiety associated with an elevated PSA, the potential complications of prostate biopsy and the risks of over detection and over treatment of prostate cancer.

What changed my practice

It was hoped that some of the controversy around PSA screening would be put to rest with the completion of two large prospective randomized trials. Interim analyses were published from both trials in 2009. The Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial randomized 76,693 men in 10 U.S. centres to PSA screening versus “usual practice”. The analysis after a median of 7 years revealed no difference in rates of survival from prostate cancer.¹

The European Randomized Study of Screening for Prostate Cancer (ERSPC) randomized 182,000 men in 7 countries to screening versus no screening. This trial revealed a 20% decrease in mortality from prostate cancer after a median of 9 years in the screening arm.²

The PLCO study is criticized for the high contamination in the “usual practice” group – 52% of patients in this arm received PSA screening during the study. Also, the follow-up was relatively short. The European study is criticized because screened patients were more likely to have their prostate cancer treated at a tertiary care centre, although the authors have shown that cancers were treated similarly when adjustments are made to control for the stage distribution. The biggest point of contention in this study, however, is that 1410 patients needed to be screened and 48 needed to be treated to save one death from prostate cancer. These numbers are comparable with the numbers needed to screen for other cancers (for example: 800-1700 for mammography and 1200 for fecal occult blood to prevent one death from breast and colorectal cancer, respectively). The number needed to treat, however, is very high, and compares unfavourably with breast cancer, for example, which is generally estimated between 10 and 15.

What I do now

The controversy around PSA screening persists, as the studies are interpreted by different parties as either supporting or detracting from the argument for prostate cancer screening. The mandate remains in large part the same – we must provide our patients with the necessary facts for them to make an informed decision whether they would like to be screened or not – but we now have much higher quality information to offer our patients in this decision process.

From the urologist’s perspective, it would appear that two key factors on the horizon are going to swing the pendulum strongly in favour of PSA screening: 1.) As the screening studies mature, the numbers needed to screen and to treat are going to come down markedly, as is evident in a recent publication from Sweden³, so that the cost, both in financial terms and with regard to potential patient morbidity from screening, will be drastically reduced; and 2.) We must learn to disconnect the diagnosis of prostate cancer from its automatic treatment. Many patients that we have treated with surgery or radiation therapy in the past are suitable for active surveillance. If we are able to limit treatment to only those cancers that need treatment in order to enhance the quality and longevity of the individual patient’s life, PSA screening will become a more valuable tool.

References: (Note: Article requests require a login ID with the BC College of Physicians website or with UBC)

1. Andriole GL, Bostwick DG, Brawley OW, et al: Effect of dutasteride on the risk of prostate cancer. N Engl J Med 362:1192-202, 2010 (View Article with CPSBC or with UBC )
2. Schroder FH, Hugosson J, Roobol MJ, et al: Screening and prostate-cancer mortality in a randomized European study. N Engl J Med 360:1320-8, 2009 (View Article  with CPSBC or with UBC)
3. Hugosson J, Carlsson S, Aus G, et al: Mortality results from the Goteborg randomised population-based prostate-cancer screening trial. Lancet Oncol, 2010 (View Article with CPSBC or with UBC)

What I did before

The management of acute ischemic stroke in the emergency department has been a contentious issue since the publication of the NINDS trial showing that thrombolysis is beneficial in selected patients, if given under three hours from onset1. This trial has received considerable debate, largely due to the fact that it was a single randomized trial of 624 patients that significantly changed how acute ischemic strokes were treated – but the therapy potentially had significant, severe side effects.

Opinion leaders in emergency medicine were largely against this therapy, due to the fact it was a single trial with modest benefit, from specialized centers (not reproducible in most institutions), with significant baseline differences between the intervention and control groups, and that it excluded older patients.2-4 Arguably, hesitation in adopting the widespread application of thrombolysis for acute ischemic stroke as standard of care had legitimate grounds, prior to September 2008.

What changed my practice

In September 2008, the ECASS III trial was published, that confirmed and reinforced the effectiveness of thrombolysis (namely alteplase) in treating acute ischemic stroke.5 This was a study of 821 patients, randomized to receive alteplase or placebo, between 3 and 4.5 hours after the onset of a stroke. Set in Europe, the median time to administration of alteplase was 4 hours. 52.4% of patients given alteplase versus 45.2% given placebo had a ‘favorable outcome’ (defined as little or no disability) (95% confidence interval 1.02 to 1.76; p=0.04). Despite the fact that the incidence of any intracranial hemorrhage and symptomatic intracranial hemorrhage was significantly higher in the alteplase group than the control group; mortality did not differ between the two groups (7.7% mortality in alteplase versus 8.4% in control; p=0.68).

This trial was the first randomized trial since the NINDS trial to show benefit from the administration of a thrombolytic in acute ischemic stroke, and extended the time window of therapy up to 4.5 hours after the onset of stroke symptoms.

What I do now

As an emergency physician, the management of patients with acute ischemic stroke has changed significantly.

1. Public awareness and activation of emergency health services: The largest reason for ineligibility of administration of a thrombolytic in acute ischemic stroke is time delay; patients arrive too late and do not call 9-1-1. Education of the public, and targeted education of patients at high risk of stroke by their primary care physicians, could increase the number of stroke patients who arrive to emergency departments within the time window for assessment. Family physicians should emphasize that patients presenting with or calling in with features to suggest a stroke should be immediately triaged to the emergency department, rather than waiting to get into the family physician’s office.

2. “Code Stroke” Triage: Acute stroke in the emergency department is now treated with the highest urgency. Often, emergency department staff and stroke teams are notified by pre-hospital personnel, prior to patient arrival. Assessments are immediate upon arrival and stroke patients are rapidly taken to the CT scanner. In almost all institutions, the decision to thrombolyse patients is a shared decision between patients, caregivers, and treating physicians.

3. The British Columbia Stroke Strategy (BCSS) Telestroke Project:6 Certain emergency departments on Vancouver Island and in Fraser Valley are linked by videoconferencing capabilities to consulting stroke neurologists at the Victoria General Hospital and Vancouver Hospital, allowing for real-time examination of patients, review of imaging, and shared thrombolysis decision making.

Bottom Line: Thombolysis for acute ischemic stroke is a small component of comprehensive acute stroke therapy. However, there now should be no debate into its effectiveness and the widespread adoption of its use in carefully selected patients should be supported.

References: (Note: Article requests might require a login ID with the BC College of Physicians website or UBC)

1. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med 1995; 333: 1581-8. (View article with CPSBC or UBC)

2. Hoffman JR. Should Physicians Give Tpa to Patients with Acute Ischemic Stroke? Against: And just what is the emperor of stroke wearing? West J Med 2000; 173(3): 149–150. (View article with CPSBC or UBC)

3. Hoffman JR, Schriger DL. A graphic reanalysis of the NINDS Trial. Ann Emerg Med 2009; 54(3): 329-36. (View article with UBC)

4. Hoffman JR. Tissue plasminogen activator (tPA) for acute ischaemic stroke: why so much has been made of so little. MJA 2003; 179 (7): 333-334. (View article with CPSBC or UBC)

5. Hacke W, Kaste M, Bluhmki E, et al. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. N Engl J Med 2008; 359: 1317-29. (View article with CPSBC or UBC)

6. The British Columbia Stroke Strategy: Telestroke Project. Online: http://www.bcstrokestrategy.ca/emergencyAcuteCare/telestroke/index.html (Accessed: October 22, 2010). (View article)

What I did before

As a psychologist specializing in cognitive behavioural therapy (CBT), I treat depressed individuals, usually referred to me by family physicians or psychiatrists. I find CBT to be a wonderfully effective and flexible form of intervention. I have seen many individuals acquire crucial skills – behavioral activation, identification and replacement of distorted thinking, etc. – with substantial antidepressant effect. I felt very good about doing this clinical work and seeing individuals cope more effectively and recover from depressive episodes.

What changed my practice

But I also see the reality that the vast majority of depressed individuals will never have access to this form of intervention. CBT is minimally available in the public health system, and even in the private system there are a limited number of psychologists with adequate training in this therapy. And there is a financial barrier, although CBT works more quickly and is therefore less expensive than other forms of psychotherapy. About 10 years ago, I began to work with a mental health services research group dedicated to improving the way mental health care is delivered. I had the opportunity to develop an alternative approach to delivering CBT-based intervention for depression.

What I do now

Working with other researchers and clinicians, I produced a series of self-management workbooks designed to teach depressed individuals evidence-based skills for mood management, available for free download from our website (http://www.comh.ca/selfcare/). Rather than focusing my practice only on individual patients, I was able to deliver a low intensity CBT intervention to a very large number of people, many times more than I could ever treat individually. This involved a trade-off: the large clinical effect I get working with an individual vs. the smaller clinical effect from self-management teaching delivered to a vast number of people. Just to give a sense of the numbers reached by this intervention, about 80,000 of the self-management workbooks have been downloaded in the last six years and about 50,000 have been distributed by provincial ministries, health agencies or other organizations. To make this intervention more effective, we developed training modules for family physicians: about 700 BC family physicians have been trained to help their patients access the workbook and use antidepressant skills.

The message is that innovative forms of service delivery have the potential to greatly expand the scope of depression intervention. But where a powerful nonpharmacological intervention is sought, treatment by a well-trained CBT psychologist remains the gold standard.

References: (Note: Article requests might require a login ID with the BC College of Physicians website or UBC)
Bilsker, D., Anderson, J., Samra, J., Goldner, E.M., & Streiner, D. (2008). Behavioural interventions in primary care. Canadian Journal of Community Mental Health, 27, 179-189. (View article with CPSBC or UBC)

Gellatly, J., Bower, P., Hennessy, S., Richards, D., Gilbody, S & Lovell, K. (2007). What makes self-help interventions effective in the management of depressive symptoms? Meta-analysis and meta-regression. Psychological Medicine, 37, 1217-1228. (View article with CPSBC or UBC)

McKendree-Smith, N.L., Floyd, M., & Scogin, F.R. (2003). Self-administered treatments for depression: a review. Journal of Clinical Psychology, 59, 275–28. (View article with CPSBC or UBC)

What I did before

The treatment of Crohn’s disease has, for the most part up until recently, been centred on controlling clinical symptoms associated with this disease.  The reason behind this approach is largely due to the fact that we did not have therapy that could change in a reliable way the inflammatory response leading to the abnormal function of the GI tract causing the symptoms of Crohn’s disease.  A mainstay of treatment was Prednisone, as this does consistently improve clinical symptoms associated with Crohn’s disease.  Unfortunately, it has been known that it has no impact on changing the natural history of Crohn’s disease, specifically a reduction in surgeries or hospitalizations.  We have always known the side effects and toxicities associated with steroid use.  What has become more concerning in recent prospective cohort studies has been an increase in mortality and infections in patients with Crohn’s disease exposed to Prednisone.

What changed my practice

As we have learned more behind the abnormal immunological response triggering inflammation associated with Crohn’s disease, medications have been developed to specifically address this problem.  The most effective medications for treating Crohn’s disease are anti-TNF inhibitors.  Infliximab and Adalimumab are the two medications in this class available in Canada.  They have been shown, like Prednisone, to quickly induce clinical remission.  Unlike Prednisone, they have also been shown to keep patients in a long-term clinical remission.  The most unique result in the clinical trials evaluating these medications has been the ability of both agents to heal the bowel.  We have known for a long time that, although Prednisone makes patients feel better, it has no impact on what the bowel looks like.  It has always been assumed, but now it has been proven, that healing the bowel changes the natural history of this disease by reducing the need for surgeries, fistula formation and hospitalization.  These medications have also shown the ability to reduce the requirement of Prednisone in patients with Crohn’s disease.

What I do now

A goal in treating patients with Crohn’s disease is to return their quality of life back to its normal state, with the avoidance of Prednisone.  I counsel each patient when I first diagnose them with Crohn’s disease that in this era we are now more than ever able to effectively treat their Crohn’s disease to the point where it should have very little, if any, impact in their life.  Effectively treating the inflammation in patients with Crohn’s disease has now allowed us to treat not just the symptoms associated with Crohn’s disease, but the disease itself.  My take home message to anyone involved in the care of patients with Crohn’s disease is to refer patients with Crohn’s disease to a gastroenterologist to review their treatment plan if the patient’s quality of life is impaired by their symptoms attributed to this disease.  Furthermore, when patients are doing well encouraging compliance for adhering to their treatment plan is important to maintain their quality of life.

References:
Rutgeerts et al. Comparison of scheduled and episodic treatment strategies of infliximab in Crohn’s disease.Gastroenterology 2004;126:402-413

Rutgeerts P et al. Adalimumab Induces and Maintains Mucosal Healing in Patients with Moderate to Severe Ileocolonic Crohn’s Disease — First Results of the EXTEND Trial.  Gastroenterology 2009;136(5 Suppl 1):A-116.

In the past 15 years there has been a rapid expansion of information about thyroid dysfunction in pregnancy. In 2007 an international task force published guidelines for management (1).

Overt hypothyroidism is seen in 0.3 to 0.5% of the general population and subclinical hypothyroidism (high TSH and normal free T4) is seen in 2-3%. Thyroid antibodies are identified in 5-15% of women.

1. What changes occur in the maternal thyroid during pregnancy?

Pregnancy increases the metabolism and clearance of thyroxin. In normal subjects thyroid production from the gland increases to maintain normal values. Patients with hypothyroidism cannot increase thyroid production and the dosage of thyroxin must be monitored and increased. The increased dosage requirement is seen as early as six weeks gestation and continues to rise until 18-20 weeks. It may increase by 30 to 50% over the non-pregnant dosage. It is then stable for the rest of the pregnancy. In pregnancy the full replacement dose is 2.0-2.4 ug/kg bw.d (per kg of body weight per day).

2. Does thyroid hormone cross the placenta to the fetus?

Maternal thyroid hormone does cross the placenta and is the only source of thyroxin for the fetus until fetal thyroxin is produced at 18-20 weeks.

3. Is maternal thyroid hormone important for fetal development?

In the first 18 weeks of pregnancy maternal thyroxin is essential for normal brain development. Maternal hypothyroidism does result in impaired mental function in the child and this is reported even in mild hypothyroidism (2).

4. Does the normal range for thyroid function tests change during pregnancy?

In normal subjects TSH declines in the first trimester. This is caused by the thyrotropic activity of HCG. The normal range is 0.03 to 2.5 mIU/l. In the second trimester the upper normal for TSH increases to 3.5mIU/l. The free T4 increases to the upper limit of the normal range in the first trimester.

5. How do we monitor the hypothyroid patient on thyroid supplement?

In hypothyroid women the dose of replacement should be monitored before a planned pregnancy to ensure a TSH of 0.3 to 2.5 mU/l. There are two options for therapy in pregnancy. One can educate the patient to increase the pre-pregnant dose by two pills per week when the pregnancy test is positive or alternately monitor the TSH at 4-6 weeks gestation and adjust the dose accordingly (3). The TSH should be monitored every 4 weeks until 20 weeks and then every 8 weeks. The goal of therapy is to maintain a TSH at less than 2.5 mIU/l

The diagnosis of hypothyroidism in pregnancy calls for immediate and aggressive replacement. After delivery the mother reverts to pre-pregnancy dosage.

6. Should all pregnant women have a TSH test?

There is controversy about doing a TSH as a screening test. The endocrine and obstetrical literature is divided between case finding and screening. It is documented that case finding alone will miss about 20% of patients with hypothyroidism. In my opinion a TSH is justified as a routine test in the first trimester. Maternal and fetal health are at risk and I think it is an appropriate screen.

7. Are thyroid antibodies of any significance?

The presence of maternal antibodies (anti-thyroid peroxidase) is often associated with hypothyroidism. The risk of post-partum thyroid disease is also dramatically increased in subjects with thyroid antibodies and in some studies is as high as 50%. Once again there is no consensus about this test as a screen I think it is justified as a onetime test in the first trimester. Many pregnant women have positive antibody titers but are euthyroid. They should be monitored during pregnancy because they are at increased risk of thyroid failure.

There is an increased risk of pregnancy complications in subjects with positive titers even when hypothyroidism is not evident (4).

8. What are the risks of maternal hypothyroidism for the pregnancy?

The risk of pregnancy complications is markedly increased in patients with untreated overt hypothyroidism. Spontaneous first trimester loss, perinatal death, abruption, eclampsia, prematurity and impaired intellectual development are all increased in maternal hypothyroidism. Subjects with subclinical hypothyroidism in the first 20 weeks of pregnancy are also at risk for pregnancy complications (5,6). These risks are dramatically reduced by proper management.

Over the past 15 years there have been major advances in our understanding of the deleterious effects of thyroid dysfunction on pregnancy. The stakes for mother and babe are high and demand appropriate monitoring and therapy.

References: (Note: Article requests might require a login ID with the BC College of Physicians website or UBC)

1. Abalovich M et al. Management of thyroid dysfunction during pregnancy and post-partum: an Endocrine Society clinical practice guideline., The Journal of Clinical Endocrinology and Metabolism 92: (suppl): S1-47, 2007. (View article with CPSBC or UBC)

2. Haddow JE et al. Maternal thyroid deficiency during pregnancy and subsequent neuropsychological development of the child, New England Journal of Medicine 341: 549-555, 1999. (View article with CPSBC or UBC)

3.Yassa l et al. Thyroid hormone early adjustment in pregnancy (The Therapy Trial), Journal of Clinical Endocrinology and Metabolism 95:3234-3241, 2010. (View article with CPSBC or UBC)

4. Stagnaro-Green A. CLINICAL REVIEW: Maternal thyroid disease and pre-term delivery, Journal of Clinical Endocrinology and Metabolism 94:21-25, 2009. (View article with CPSBC or UBC)

5. Casey B et al. Subclinical hypothyroidism and pregnancy outcomes, Obstet Gynecol 105:239-245, 2005. (View article with CPSBC or UBC)

6. Smallridge RC and Ladenson P.W. Hypothyroidism in pregnancy: Consequences to neonatal health, Journal of Clinical Endocrinology and Metabolism 86:2349-53, 2001. (View article with CPSBC or UBC)

What I did before

I direct an outpatient clinic that treats patients with chronic leg ulcers. The majority of these wounds are venous in origin with some diabetic foot ulcers and pressure sores. The vast majority of patients do well with so-called ‘Best Clinical Practice’; however, it is not unusual for some ulcers to be very stubborn. In many cases, this failure to heal is characterized by the lack of development of healthy granulation tissue. The majority of these ulcers lacking granulation tissue have, instead, yellow/green, slimy, odourous material on the base. Despite this, we would try to facilitate proper moisture balance by applying modern wound dressings. Unfortunately, when this slimy material is prevalent, healing is impaired.

What changed my practice

I have always wondered just what that yellow slimy material was in the wound base. Yellow in the wound can signify different things. Fibrin presents as a gel usually on the base of venous leg ulcers. Yellow slough represents hydrated necrotic tissue and has the consistency of leather. We observed that when this yellow/green coloured slimy material persists, the wound does not heal and granulation tissue either does not develop or disappears.

One day, while flying to Toronto, I read an article in the Scientific American magazine I purchased at the airport. It was a review article by William Costerton, the man who coined the term, ‘Biofilm’, in 1979. He described the structure, formation, and the polymicrobial nature of biofilms in nature. In nature, biofilms often have the consistency of slime and it made sense that they could develop in a chronic wound. Furthermore, it seemed perfectly reasonable that this complex matrix of multiple species of bacteria could successfully compete with host immune defense and prevent healing. It also seemed logical that this material should be removed regularly in order to enhance healing. After all, if plaque, a prototypical biofilm of teeth, needs to be removed daily in order to avoid tooth decay and periodontal disease, wound biofilms would need to be regularly debrided to promote healing.

What I do now

The concept of biofilm in chronic wounds is in its infancy at the present time. It is just now being proposed that they play an important role in the pathogenesis of non-healing. It is also known that they are very resistant to treatment by systemic or topical antibiotics. Antimicrobial dressings, often consisting of sliver derivatives, are also unable to significantly impede biofilms. At the Wound Healing Clinic, we believe that almost every one of our poorly-healing leg ulcers possesses a healthy thriving biofilm. We now, routinely, debride biofilms using a disposable curette after providing topical local anesthesia (2% xylocaine gel applied under gauze for 10 minutes). I use the dull side of the curette to avoid cutting. Since the synonym for biofilm is ‘slime’, cutting and aggressive scraping are not required. Biofilms are extremely tenacious and so debridement must be relentless and repeated weekly at least. Although the biofilm usually returns quite quickly, eventually it ‘gives up’ and does not return. This is followed by rapid healing. Since we, at the Wound Healing Clinic, have instituted this form of debridement as part of wound bed preparation, better clinical outcomes have been realized.

References: (Note: Article requests might require a login ID with the BC College of Physicians website or UBC)

1. Costerton, W. Battling Biofilms. Scientific American July 2001. (View article with CPSBC or UBC)
2. James GA, et al. Biofilms in chronic wounds. Wound Rep Reg 16,37-44,2008. (View article with CPSBC or UBC)
3. Bjarnsholt T, et al. Why chronic wounds will not heal: a novel hypothesis. Wound Rep Reg 16,2-10,2008. (View article with CPSBC or UBC)
4. Cardinal M, et al. Serial surgical debridement: A retrospective study on clinical outcomes in chronic lower extremity wounds. Wound Rep Reg 17,306-311,2009. (View article with CPSBC or UBC)

*With special thanks to Dr. Bonnie Dobbs, Director, The Medically At-Risk Driver Centre Director of Research, Division of Care of the Elderly, Professor, Department of Family Medicine for her support and guidance regarding research.

What I did before
Despite recent articles^1,2, I had always felt uncomfortable about knowing what was the best way to screen medically at risk patients’ fitness to drive. In the past I would use a combination of history, collateral information, and other cognitive screening tests, the results from a DriveABLE exam, or referral to a medical consultant for their opinion.

What changed my practice
Since the introduction of the new 2010 BC Guide in Determining Fitness to Drive in July 2010  (see http://www.pssg.gov.bc.ca/osmv/publications/docs/2010-guide-in-determining-fitness-to-drive.pdf) and the change in the referral and reimbursement process for DriveABLE examination by the BC OSMV, I have tried to change my practice to include these new Guidelines, the use of the SIMARD MD, and referral to the OSMV for further direction.

What I do now
If I had to share the top 5 important points that I have learned about from reviewing and learning from colleagues, attending presentations, and reviewing data on assessing Driver’s Fitness, they would be:

1)      With the increasing number of aging patients in our population, there is also an increasing number of dementia cases diagnosed each year³.  When equated for exposure (e.g., amount of kilometers driven), increasing age⁴ and the presence of medical conditions⁵ increases fatality rates due to motor vehicle crashes, as well as at-fault crash rates respectively. Importantly, it’s not age per se, but rather the presence of medical conditions such as neurological, renal, and endocrine issues that affect driving competency. Many illnesses affect driving competency due to their impact on cognitive functioning. The new 2010 OSMV guidelines have an easy-to-use table (p.85) which identifies medical conditions which may affect cognition. There are also patient screening questionnaires which can be used in family practice.⁶

2)      According to the current BC Motor Vehicle Act, a physician has a legal responsibility to report patients with medical conditions that affect driving ability to the OSMV. Based on case law⁷, physicians can be held legally liable for NOT reporting patients at risk. Finally, the current BC Motor Vehicle Act protects physicians from legal action from patients if the reporting is done in good faith.

3)      In primary care, we need a short, inexpensive or free, easy to administer, easy to score and scientifically valid screening test to determine which of our medically at-risk patients would benefit from further assessment of driver’s fitness. The SIMARD MD⁸ is a published Screening tool for the office based Identification of cognitively impaired Medically At Risk patients which has been adopted by the OSMV as a screening test for medically at-risk drivers to be used by primary care providers.  Compared to other commonly used cognitive assessment tests that we use to screen for dementia such as the MMSE⁹, the SIMARD MD is a better predictor of results from an on-road assessment. The use of dual cutpoints allows physicians to identify:

a.  those patients most likely to fail the on-road assessment (lower cutpoint),

b.  those patients most likely to pass an on-road assessment (upper cutpoint), and

c.  those classified as indeterminate (in need of a DriveABLE Assessment for determination of driving competency).

Importantly, the SIMARD MD does not replace clinical judgment. Rather, the results of the SIMARD MD should be used in conjunction with clinical findings for decisions related to determination of driving competency.

4)      In terms of physician reimbursement, although there are ongoing fee negotiations between the British Columbia Medical Association, Society of General Practitioners of BC, and the government, there are ways to bill either privately or publically for the Driver’s Medical Examinations¹⁰. Furthermore, if medically indicated and necessary and if the documentation and  visit is sufficient, physicians can bill the age appropriate 0100 fee codes and can access the mental health planning fee code 14043.  To report a patient’s SIMARD results or safety issues affecting driving, I use either the space provided to me in the comments section of the DMER forms or a standardized letter to the licensing authority¹¹.

5)      The BC College of Family Physicians, BC OSMV, and the British Columbia Automobile Association (BCAA) Traffic Safety Foundation are working to help educate family physicians as well as streamline the process for patients to have the DriveABLE examination.  The BCAA Traffic Safety Foundation helps to co-ordinate these tests and the reporting of results to family physicians. However, only the OSMV has the right to revoke patients driver’s licenses. In cases where patients’ may need to go on for further tests, I provide them supportive counseling and also provide them with information and links to community resources as this is a significant loss and perceived threat to their independence ¹²

Billing codes: www.sgp.bc.ca

The October 2010 Billing tip is on billing of the DMER:
Drivers’ Medical Certification
1.         Drivers Medicals for Patients with Medical Conditions
When completing these forms (blue stripe), the examining physician has the ability to choose to bill the patient the entire BCMA recommended rate or to bill OSMV via teleplan $75.00 and balance bill the patient the difference of the rate that they wish to set for this service.  When billing for patients with medical conditions, the following fee codes are billable:
96220               OSMV Driver’s Medical Examination Report (DMER) for any driver with a known or possible medical condition (may bill part to OSMV via teleplan)
96221               OSMV Diabetic Driver Report-stand alone (no DMER): Diabetic Driver Report for commercial drivers with diabetes – known medical condition  (may bill part to OSMV via teleplan)

96222               OSMV Diabetic Driver Report sent out with DMER: Diabetic Driver Report for commercial drivers with diabetes – known medical condition (may bill part to OSMV via teleplan)

2.         Drivers Medicals For Patients 80 years of age and over (yellow stripe)
This form is completed when determining medical fitness for driving for patients 80 years and over.

3.         Drivers Medicals for other categories (Class 1, 2 & 3) (yellow stripe)
This form is completed when determining medical fitness for patients who have applied for or for continuation of Class 1, 2 or 3 Drivers Licenses.
When determining the medical fitness of patients presenting with either of the forms with a yellow stripe, nothing is billable directly to MSP or OSMV.  The patient, or in some cases their employer, is responsible for payment for this service.  The fee code for this service is dependent on the nature of the examination requested by OSMV.  If a full physical examination is requested and provided, then the 00055 fee is billed.  In the case of those patients where a limited examination is requested and provided, the 00056 fee is the appropriate billing.
00056               Driver’s License – limited exam.
00055               Driver’s License – full exam

References: (Note: Article requests might require a login ID with the BC College of Physicians website or UBC)

1) D Hogan, Which older patients are competent to drive? Approaches to office-based assessment Can Fam Physician 2005; 51; 362-368. http://www.cfp.ca/cgi/reprint/51/3/362

2) F Molnar et al, Approach to Assessing fitness to drive in patients with cardiac and cognitive conditions Can Fam Physician Nov 2010; 56; 1123-9. http://www.cfp.ca/cgi/reprint/56/11/1123

3) Rising Tide: The Impact of Dementia on Canadian Society (Alzheimer Society of Canada, 2010) http://www.alzheimer.ca/english/rising_tide/rising_tide_report.htm

4) Insurance Institute for Highway Safety. Driver fatality rate by age. Available from: http://www.iihs.org/research/fatality_facts_2006/olderpeople.html

5) E Diller et al. Evaluating drivers licensed with medical conditions in Utah, 1992-1996. DOT HS 809 023. Washington, DC: National Highway Traffic Safety Administration (1999).  http://ntl.bts.gov/lib/25000/25900/25974/DOT-HS-809-023.pdf

6) The Medically At-Risk Driver Protocol Working Group. Assessing the Medically At-Risk Driver – The Medically At-Risk Driver Protocol, Tools, and Resources for Health Care Professionals. Contact www.mard.ualberta.ca

7) Freese v Lemmon, 210 NW 2d 576, 577-578, 580 (Iowa 1973)

8) BM Dobbs & D Schopflocher. The introduction of a new screening tool for the identification of cognitively impaired medically at-risk drivers: The SIMARD A Modification of the DemTect. Journal of Primary Care and Community Health, 2010, 1(2), 119-127. (View article with UBC or request it with CPSBC) SIMARD MD tool: http://www.mard.ualberta.ca/Home/SIMARD/tool.cfm

9) www.sgp.bc.a Tutorial online for information on billing DMER and other fees

10)http://www.drivesafe.com/MV%202351%20(07%2009)%20Report%20of%20a%20Condition%20Affecting%20Fitness%20and%20Ability%20to%20Drive.PDF

11) Patient Resources/Physician Resources:

1) BCAA Traffic Safety Foundation www.driverfitnessbc.com 3020 Beta Avenue, Burnaby, BC V5G 4K4. Phone:604-298-5107 Fax:604-298-6497; Email: trafficsafety@tsf-bcaa.com

2) BC Transit 604-953-3333 or google www.bctransit.com and enter your community

3) HandyDART Program http://www.translink.ca/en/Rider-Info/HandyDart.aspx. For clients with a physical or cognitive disability who are unable to use public transit without assistance. Application available online or contact Access Transit at 778-452-2860.

4) HandyCard and Taxi Savers Program: http://www.translink.ca/en/Rider-Info/Accessible-Transit/HandyCard-Taxi-Saver.aspx. Available to clients with a physical or cognitive disability who can’t use public transit without assistance.

• HandyCard lets clients travel for the “concession” rate on public transit and a person accompanying them to provide assistance can travel for free.

• Taxi Savers are available to clients who have a HandyCard. They provide discounted rates for a taxi from any company of the clients’ choice. Application available online or contact Access Transit at 778-452-2860.

5) Volunteer Driver Program, VCH: 604-267-2678. Must be a client of VCH. Transportation for medical appointments only.

6) Provincial Based Private Companies

A) Driving Miss Daisy http://www.drivingmissdaisy.net/, 1-877-613-2479. Offers transportation at an hourly rate to medical appointments, social engagements, and other events. Services offered in selected cities across BC

B) We Care Medi-Transit www.wecarehealth.com, 604-264-9003. Offers transportation at an hourly rate to medical appointments, social engagements, and other events. accompany clients by taxi or in the service provider’s own car.

7) Lower Mainland

A) Special Needs Transport: www.sntransport.ca, 1-800-768-0044. Door to door service for medical appointments or social engagements.

B) Veterans Independence Program: http://www.servicecanada.gc.ca/eng/goc/vip.shtml, 1-866-522-2122. Must be a veteran registered with Veterans Affairs Canada (or provide care to someone who is). Offers transportation for shopping, banking, visiting friends, etc.

C) Alzheimer’s Society of BC Dementia Helpline, Tuesday to Friday, 10am-4pm, 604-681-8651 or 1-800-936-6033, supportline@alzheimerbc.org

What care gaps I noticed

I recently had to review the data on long term outcomes for survivors at extremely low birthwt (<800 g) or extreme prematurity (<26 wks). An article from our own institution and another showed me some gaps in care that I had not been addressing and that seemed to be missed in the community as well. Prior to my review, I was missing the subtleties of disability that the ex-premature child can have and how these differences can significantly impact schooling and daily living. I was so keen to applaud any survival that I was not recognizing (and thus not providing support for) the degree of ongoing difficulties these families were facing.

What changed my practice

In my review of the outcome data, and particularily looking at data from our own institution, I was reminded that infants born at the limits of viability (< 26 wks GA or <800 g) have a significant percentage of morbidity and mortality even though not born with a syndrome or particular anomalies. We are seeing a higher percentage of extreme prematurity associated with assisted reproductive technology as a function of multiple births and risk of premature delivery in itself.

Taking from Dr. Synnes’ article, the results on morbitidity for survivors at 23-25 wks gestations are as follows:

Normal development 40% Mild impairment 30% Moderate impairment 20%

Severe impairment 10% More than 50% of children born extremely prem will have a learning disability

Negative predictive factors include: male gender, multiple births, choriamnionitis, prolonged rupture of membranes, intrauterine growth restriction and underlying genetic disorders. Even if the final outcome will be normal or mildly impaired development, these children follow their own developmental trajectory in childhood and their development may not look much like that read about in parenting advice books.

What I do now

1. Acknowledge and support the ‘survivor’ characteristic of patient and parent.

The data from these articles looks first at survival and then long term outcomes. These children are survivors as are their parents. It has amazed me how often asking about the parental experience in the

NICU can cause a parent to cry in memory even 4 years after discharge. The majority of parents have been through emotional trauma during their time in the NICU and we have 2 social workers dedicated to the NICU to help with acute stress. There is not a formal community support structure for parents of ex-prems but health caregivers can assist by recognizing the signs and symptoms of post-traumatic stress, acknowledging the stress and connecting these families with mental health supports in the community if it is needed.

2. I believe that putting the child in a survivor category creates perspective if the outcome is anything but clinically normal. As parents mourn the loss of a “normal pregnancy and birth experience”, they have a more than 50% chance of having ongoing issues dealing with an atypical childhood for their child. The word survivor helps allude to the spectrum of sensory issues these children are plagued with. Rather than being safely encased in their mother’s uterus, these children went through a number of noxious stimuli of no predictable pattern. They are often easily upset by new sensations and have a lower threshold for sensory overload. I now try and review this information with parents in the final weeks of preparing for discharge home. Our nursing staff in the NICU have been education the family from the first day about how to read an infant’s cues, judging when the child is over or understimulated, and teaching parents practical ways to help their children cope. This valuable education continues with our community Infant Development teams.

3. Provide anticipatory guidance regarding functional expectations based on evidence. From the outcome data from BCCH in the past, we know that some children with a moderate and most children with a severe disability will be unable to live completely independently as adults. Given that the final outcome may not be evident till ages 3-5, the discussion of future independence is often not addressed until later visits in the Followup Clinic. I am not adverse to the timing of this as I think that some families might be crushed by the burden of the future if they are struggling in the now. Our followup team attempts to harness as many community resources as are needed on an ongoing basis so that the family is supported in the present. Given that our followup visits end at age 4 ½, we try to make recommendations to community caregivers that will ensure continuity of support in areas such as schooling, speech and language therapy, occupational therapy and physiotherapy.

4. Address the multi-factorial nature of the potential learning disabilities. Some time after the initial crisis of the extremely premature birth is over, parents usually begin to ask questions about long term outcome. This discussion then leads to a review of outcomes, including learning disabilities, how these are defined, diagnosed and treated. We can often get an advance warning on learning disabilities in our followup clinic with our formal Psychologic assessments. We encourage parents to pay close attention to school progress and work in tandem with educators to ensure that a quiet or disruptive child is not labeled a behavioural issue when the risk of learning disabilities is so high. Another barrier to a successful educational experience is poor fine motor skills. These children print like doctors but without the speed of production! Poor fine motor skills also affect activities of daily living such as eating, tooth brushing and dressing. Parents of ex-prems are encouraged to find fun activities on a daily basis that help develope fine motor skills. The occupational therapists have a wealth of suggestions for this area.

5. Given that the NICU experience was “the most difficult struggle I have ever had in my life” (a father’s quote), we owe the family a full review of the cause of the premature birth. If the family is considering having more children, they want reassurance that we will do our best to try and prevent a premature birth in future pregnancies.

In summary, these children may “look” normal but their NICU experience has had a profound effect on them and their families. As caregivers, we want to specifically ask about potential issues and offer advocacy for these families in the community and in the schools.

References: (Note: Article requests might require a login ID with the BC College of Physicians website or UBC)

Synnes A, et al: Management of the Newborn delivered at the threshold of viability BC Med J 50 (9) 2008 (View article with CPSBC or UBC)

Latal B: Prediction of Neurodevelopmental Outcome after Preterm Birth Pediatr Neurol 40 (6) 2009 (View article with CPSBC or UBC)

How failure of consensus guidelines to impact others’ practice improved my monitoring of cardiovascular disease risk in people with chronic mental illness

What I did before

Although psychiatrists are used to treating chronic disease, they expend their effort on managing psychosis, mood disorders, and anxiety. Chronic medical disorders such as hypertension, diabetes, obesity, and the consequent vascular disease have been the realm of family physicians and internists. The evidence, however, has become impossible to ignore that people with chronic mental illness are dying from heart attacks and strokes at a higher rate than the general population. Cardiovascular disease shortens the life expectancy of people with mental illness by 20 or more years. ⁽¹⁾

In the past, I seldom paid attention to my patients’ weight, blood pressure, or exercise patterns, even though antipsychotics that I prescribed, especially olanzapine, clozapine and quetiapine, may have worsened their metabolic syndrome.

What changed my practice

In 2004, the American Psychiatric Association and the American Diabetes Association jointly issued guidelines on metabolic monitoring in patients on chronic antipsychotic therapy. ⁽²⁾ The guidelines recommend that prescribers obtain anthropometrics, including weight and waist circumference, and fasting glucose and lipid profiles at baseline and at specific intervals.

Morrato et al. looked at how often U.S. physicians are obtaining the recommended glucose and lipid testing in publicly-insured patients. ⁽³⁾ Only about a quarter of patients had serum glucose at baseline, and 10% had lipid profiles. Haupt et al. found that baseline and follow-up monitoring rates were no better in commercially insured U.S. patients. ⁽⁴⁾ In both studies, the investigators looked at testing rates before and after publication of the 2004 guidelines and found no meaningful change in practice. Both psychiatrists and family physicians are failing to monitor glucose and lipids. As for compliance with anthropometrics, no data are available.

What I do now

In the Mental Health Program at St. Paul’s Hospital in Vancouver, we are implementing a systematic approach to monitoring our patients’ metabolic risk factors. Patients admitted for inpatient treatment have anthropometric data recorded routinely, and serum glucose and lipid testing is done if no recent values are available. Most importantly, the treatment team examines the information and selects interventions appropriate to each patient. We offer education on cardiovascular risk, dietary counselling, smoking cessation interventions, referral to a family physician, or even follow-up with a preventive cardiology clinic.

I now realize that whether I am treating patients for schizophrenia, bipolar disorder, or that in-between problem called schizoaffective disorder, they probably also need intervention for weight gain, smoking, and physical inactivity. My practice is in a well-resourced academic hospital. Although more of a challenge, patients in primary care also need this monitoring and intervention. An incentive is the cardiovascular risk assessment fee, which B.C. family physicians may be able to use for preventive interventions. In treating people with chronic mental disorders, collaboration between family physicians and psychiatrists is crucial to ensure that cardiovascular risk is effectively managed.

References: (Note: Article requests might require a login ID with the BC College of Physicians website or UBC)
1. Newcomer JW, Hennekens CH.: Severe mental illness and risk of cardiovascular disease. JAMA. 2007;298:1794– 1796. (View article with CPSBC or UBC)
2. American Diabetes Association, American Psychiatric Association, American Association of Clinical Endocrinologists, North American Association for the Study of Obesity Consensus development conference on antipsychotic drugs and obesity and diabetes. Diabetes Care. 2004;27: 596– 601. (View article with CPSBC or UBC)
3. Morrato EH, Druss B, Hartung DM, et al. Metabolic Testing Rates in 3 State Medicaid Programs After FDA Warnings and ADA/APA Recommendations for Second-Generation Antipsychotic Drugs.  Arch Gen Psychiatry. 2010;67:17-24. (View article with CPSBC or UBC)
4. Haupt DW, Rosenblatt LC, Kim E, et al. Prevalence and predictors of lipid and glucose monitoring in commercially insured patients treated with second-generation antipsychotic agents. Am J Psychiatry. 2009;166:345-353. (View article with CPSBC or UBC)

What I did before

I generally inquired about smoking in my patients and tried to help them quit.  I would offer smoking cessation advice if patients were ready to accept it and proceed to offering pharmacotherapy if appropriate.

What changed my practice

I first became aware of the Canadian Tobacco Use Monitoring Survey which highlights that tobacco use remains the number one preventable cause of illness and death in our society and that tobacco kills twice as many people in BC as motor vehicle crashes, alcohol, suicide and homicide combined. I then became aware of the recent updated Guidelines of the US Public Health Service in 2008 for “Treating Tobacco Use and Dependence” which in brief states:

1. Tobacco dependence is a chronic disease.
2. It is essential that clinicians and health care systems consistently identify and document tobacco use status and treat every tobacco use seen in a health care setting.
3. Tobacco dependence treatments are effective and every patient willing to make a quit attempt should be encouraged to use recommended counseling treatments and medications.
4. Brief tobacco dependence treatment is effective.
5. Individual, group, and telephone counseling are effective and their effectiveness increases with treatment intensity.
6. Numerous effective medications are available for tobacco dependence – (5 nicotine and 2 non-nicotine).  Their use increases long-term smoking abstinence rates.
7. Counseling and medication are effective when used alone but is more effective when used in combination.
8. Telephone quitline counselling is effective.
9. For tobacco user unwilling to quit, motivational treatments can be effective in increasing future quit attempts.
10. Providing coverage for clinically effective and cost-effective tobacco dependence treatment increases quit rates.

For full text, please log onto www.surgeongeneral.gov/tobacco/treating_tobacco_use.pdf

The additional insights I have gained is that this addictive behaviour is very much hard-wired into the patient’s brain neurobiology especially if they started into tobacco use early.  Treatments may need to be life-long and at adequate doses.

I also became aware that tobacco use is particularly problematic for the mentally ill population in two ways:

• They are particularly susceptible to tobacco addiction and accounts for nearly half of the tobacco market.
• That withdrawal of nicotine in these patients can prompt exacerbation of psychiatric disorders, cause relapse, mimic or worsen medication side effects, and increase blood levels of several medications.

What I do now

This has changed my focus from episodic checking for tobacco use to systematization of the process as well as offering both the counselling and appropriate medications for patients.  I understand that even providing a brief intervention of 3 minutes will double the chance of patients quitting. Once patients express willingness to quit, referral to The Quit Now program with the telephone counselling www.quitnow.ca will assist patients with this difficult disease. I also put in more intensive effort to provide my patients with mental illness the necessary counselling, social supports and help to obtain financial coverage for effective tobacco cessation pharmacotherapy.  This group will also require closer monitoring with tobacco cessation strategies. Further information is provided by a resource developed by PHSA through www.healthyheart.bc.ca → Tobacco Intervention → Health Professionals.

Additional Reading:

Dr. Fred Bass, Special Feature: Training the Inner Alligator. BCMJ 2010; 52: 23 (Full Article)